About all

Glucose fasting 105: Is There a ‘Safe’ Blood Sugar Level? – Type 2 Diabetes

Prediabetes – Diagnosis and treatment


The American Diabetes Association (ADA) recommends that diabetes screening for most adults begin at age 45. The ADA advises diabetes screening before age 45 if you’re overweight and have additional risk factors for prediabetes or type 2 diabetes.

There are several blood tests for prediabetes.

Glycated hemoglobin (A1C) test

This test shows your average blood sugar level for the past three months. The test measures the percentage of blood sugar attached to the oxygen-carrying protein in red blood cells called hemoglobin. The higher your blood sugar levels, the more hemoglobin you’ll have with sugar attached.

In general:

  • An A1C level below 5.7% is considered normal
  • An A1C level between 5. 7% and 6.4% is considered prediabetes
  • An A1C level of 6.5% or higher on two separate tests indicates type 2 diabetes

Certain conditions can make the A1C test inaccurate — such as if you’re pregnant or have an uncommon form of hemoglobin.

Fasting blood sugar test

A blood sample is taken after you fast for at least eight hours or overnight.

In general:

  • A fasting blood sugar level below 100 milligrams per deciliter (mg/dL) — 5.6 millimoles per liter (mmol/L) — is considered normal.
  • A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 7.0 mmol/L) is considered prediabetes. This result is sometimes called impaired fasting glucose.
  • A fasting blood sugar level of 126 mg/dL (7. 0 mmol/L) or higher indicates type 2 diabetes.

Oral glucose tolerance test

This test is usually used to diagnose diabetes only during pregnancy. A blood sample is taken after you fast for at least eight hours or overnight. Then you’ll drink a sugary solution, and your blood sugar level will be measured again after two hours.

In general:

  • A blood sugar level less than 140 mg/dL (7.8 mmol/L) is considered normal.
  • A blood sugar level from 140 to 199 mg/dL (7.8 to 11.0 mmol/L) is considered prediabetes. This is sometimes referred to as impaired glucose tolerance.
  • A blood sugar level of 200 mg/dL (11.1 mmol/L) or higher indicates type 2 diabetes.

If you have prediabetes, your doctor will typically check your blood sugar levels at least once a year.

Children and prediabetes testing

Type 2 diabetes is becoming more common in children and adolescents, likely due to the rise in childhood obesity. The ADA recommends prediabetes testing for children who are overweight or obese and who have one or more other risk factors for type 2 diabetes.

These other risk factors include:

  • Family history of type 2 diabetes.
  • Race. Children who are African American, Hispanic, Native American, Asian American and Pacific Islander are at higher risk.
  • Low birth weight.
  • Being born to a mother who had gestational diabetes.

The ranges of blood sugar level considered normal, prediabetic and diabetic are the same for children and adults.

Children who have prediabetes should be tested annually for type 2 diabetes — or more often if the child experiences a change in weight or develops signs or symptoms of diabetes, such as increased thirst, increased urination, fatigue or blurred vision.


Healthy lifestyle choices can help you bring your blood sugar level back to normal, or at least keep it from rising toward the levels seen in type 2 diabetes.

To prevent prediabetes from progressing to type 2 diabetes, try to:

  • Eat healthy foods. Choose foods low in fat and calories and high in fiber. Focus on fruits, vegetables and whole grains. Eat a variety of foods to help you achieve your goals without compromising taste or nutrition.
  • Be more active. Aim for at least 150 minutes of moderate or 75 minutes of vigorous aerobic activity a week.
  • Lose excess weight. If you’re overweight, losing just 5% to 7% of your body weight — about 14 pounds (6.4 kilograms) if you weigh 200 pounds (91 kilograms) — can reduce the risk of type 2 diabetes. To keep your weight in a healthy range, focus on permanent changes to your eating and exercise habits.
  • Stop smoking. Smoking may up your risk of developing type 2 diabetes.
  • Take medications as needed. If you’re at high risk of diabetes, your doctor might recommend metformin (Glumetza, others). Medications to control cholesterol and high blood pressure might also be prescribed.

Children and prediabetes treatment

Children with prediabetes should undertake the lifestyle changes recommended for adults with type 2 diabetes, including:

  • Losing weight
  • Eating fewer refined carbohydrates and fats, and more fiber
  • Reducing portion sizes
  • Eating out less often
  • Spending at least one hour every day in physical activity

Medication generally isn’t recommended for children with prediabetes unless lifestyle changes aren’t improving blood sugar levels. If medication is needed, metformin (Glumetza, others) is usually the recommended drug.

Clinical trials

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition.

Alternative medicine

Many alternative therapies have been touted as possible ways to treat or prevent type 2 diabetes. But, there’s no definitive evidence that any alternative treatments are effective. Therapies that have been said to be helpful in type 2 diabetes and are also likely to be safe, include:

  • Cassia cinnamon
  • Flaxseed
  • Ginseng
  • Magnesium
  • Oats
  • Soy
  • Xanthan gum

Talk to your doctor if you’re considering dietary supplements or other alternative therapies to treat or prevent prediabetes. Some supplements or alternative therapies might be harmful if combined with certain prescription medications. Your doctor can help you weigh the pros and cons of specific alternative therapies.

Preparing for your appointment

You’re likely to start by seeing your primary care doctor. He or she may refer you to a doctor who specializes in diabetes treatment (endocrinologist), a dietitian or a certified diabetes educator.

Here’s some information to help you get ready for your appointment.

What you can do

Before your appointment, take these steps:

  • Ask about any pre-appointment restrictions. You’ll probably need to fast for at least eight hours before your appointment so that your doctor can measure your fasting blood sugar level.
  • List symptoms you’ve been having and for how long.
  • List all medications, vitamins and supplements you take, including the doses.
  • List key personal and medical information, including other conditions, recent life changes and stressors.
  • Prepare questions to ask your doctor.

For prediabetes, some basic questions to ask your doctor include:

  • How can I prevent prediabetes from turning into type 2 diabetes?
  • Do I need to take medication? If so, what side effects can I expect?
  • I have other health conditions. How can I best manage them together?
  • How much do I need to exercise each week?
  • Should I avoid any foods? Can I still eat sugar?
  • Do I need to see a dietitian?
  • Can you recommend any local programs for preventing diabetes?

What to expect from your doctor

Your doctor is likely to ask you a number of questions, such as:

  • Has your weight changed recently?
  • Do you exercise regularly? If so, for how long and how often?
  • Do you have a family history of diabetes?

Sept. 22, 2020

Prediabetes 101

Misconceptions abound about prediabetes. Elizabeth Halprin, MD, an endocrinologist at Joslin Diabetes Center in Boston, explains some basics about this condition.

How is prediabetes different from diabetes?

Prediabetes is a condition that happens when your blood sugar levels are above normal but not high enough to be considered type 2 diabetes. A fasting blood sugar between 110 and 125 would be considered in the “prediabetes” range. Less than 110 is normal and greater than 126 is diabetes. These abnormal blood sugar levels usually happen when a person’s tissues don’t respond well to a hormone [insulin] signal to take up sugar from the blood. Also, the body doesn’t make enough insulin to help overcome the weak tissue response to insulin.

Does prediabetes always progress to type 2 diabetes?

No, not always. People who eat a health-conscious diet, exercise regularly, and keep a healthy weight can lower their blood sugar levels and even bring them back to normal. In fact, learning you have prediabetes gives you a chance to make the lifestyle changes you need to avoid getting type 2 diabetes.

What puts me at risk of having prediabetes?

The biggest risk factor for prediabetes in the general adult population is being overweight or obese, particularly when the extra weight is due to excess fat in your abdomen. Also, the older you get, the higher your risk goes. Black, Hispanic, and Asian people are at higher risk than other races, as well as women who have had gestational diabetes, and people with a family history of diabetes.

How can a doctor tell if I have prediabetes? Are there symptoms?

There’s no way to know you have prediabetes without a doctor diagnosing with a blood test. Typically, people with prediabetes don’t have any symptoms. Symptoms of high blood sugar levels — like frequent urination, increased thirst, blurry vision, and fatigue — usually become noticeable once a person develops diabetes. Some people with prediabetes may have signs of insulin resistance — darkened skin in the armpit or on the back and sides of the neck or small skin growths or skin tags in these same areas.

What can I do to help prevent prediabetes?

Eat more vegetables, fewer simple carbs [such as those in sugary foods like candy and many processed foods], and increase your activity. Try to get 10,000 steps per day, at least. Exercise gets your body to use its own insulin more efficiently so that the blood sugars come down. It also helps you lose or maintain your weight, which will decrease the risk of prediabetes and diabetes.

Avoid junk food, and sweets, and especially sweet drinks like soda and juice. Get plenty of sleep. Poor sleep hygiene and not getting enough sleep makes it harder to lose weight, and therefore increases the risk of prediabetes.

Find more articles, browse back issues, and read the current issue of WebMD Magazine.

The Surprising Truth About Prediabetes

Prediabetes Flies Under the Radar

You can have prediabetes for years but have no clear symptoms, so it often goes undetected until serious health problems show up. That’s why it’s important to talk to your doctor about getting your blood sugar tested if you have any of the risk factors for prediabetes, which include:

  • Being overweight
  • Being 45 years or older
  • Having a parent, brother, or sister with type 2 diabetes
  • Being physically active less than 3 times a week
  • Ever having gestational diabetes (diabetes during pregnancy) or giving birth to a baby who weighed more than 9 pounds

Race and ethnicity are also a factor: African Americans, Hispanic/Latino Americans, American Indians, Pacific Islanders, and some Asian Americans are at higher risk.

Ready to find out your risk? Take the 1-minute prediabetes risk test and be sure to share the results with your doctor.

Diabetes Is Harder to Live with Than Prediabetes

Though people with prediabetes are already at a higher risk of heart disease and stroke, they don’t yet have to manage the serious health problems that come with diabetes.

Diabetes affects every major organ in the body. People with diabetes often develop major complications, such as kidney failure, blindness, and nerve damage (nerve damage can lead to amputation of a toe, foot, or leg). Some studies suggest that diabetes doubles the risk of depression, and that risk increases as more diabetes-related health problems develop. All can sharply reduce quality of life.

Prediabetes = Preventdiabetes

Think of prediabetes as a fork in the road: Ignore it, and your risk for type 2 diabetes goes up. Lose a modest amount of weight and get regular physical activity, and your risk goes down. Modest weight loss means 5% to 7% of body weight, just 10 to 14 pounds for a 200-pound person. Regular physical activity means getting at least 150 minutes a week of brisk walking or similar activity. That’s just 30 minutes a day, five days a week.

The CDC-led National Diabetes Prevention Program (National DPP) has been proven to help people make the lifestyle changes needed to prevent or delay type 2 diabetes. Through the program, participants:

  • Work with a trained coach to make lasting lifestyle changes.
  • Discover how to eat healthy and add more physical activity into their day.
  • Find out how to manage stress, stay motivated, and solve problems that can slow progress.

If you’re told you have prediabetes, ask your doctor or nurse if there is a National DPP lifestyle change program offered in your community. The best time to prevent type 2 diabetes is now.

Gestational Diabetes Fasting Blood Sugar 105-110

If you’re diagnosed with gestational diabetes (GD), it’s very important to keep your blood glucose (sugar) level within the target range. You may need to check it several times a day – typically before meal (fasting) and after meal. Fasting blood sugar 105 and 110 mg /dL are commonly considered abnormal. These high levels are still too dangerous for pregnancy. The good news, GD is controllable and you can still have a healthy pregnancy.

Brief summary about gestational diabetes

As the name suggests, it occurs during pregnancy – and it’s only found in pregnancy. You cannot get rid of it during pregnancy, but again it’s treatable! And it usually goes away on its own after giving birth.

Causes and risk factors

Like diabetes mellitus, in GD the body also loses its natural ability to use glucose (sugar) for energy as effectively as usual. What is the exact cause? The answer is not fully known yet. But there are some explanations.

The increased pregnancy hormones, especially in late pregnancy, are often to blame. The placenta is essential part of pregnancy. It is responsible to stimulate and produce essential hormones for baby development and growth during pregnancy.

But some of these hormones can interrupt with the mother’s insulin that may cause a condition called insulin resistance (when insulin doesn’t work as effectively as usual). The demand for insulin can significantly increase during pregnancy, could be 2-3 times greater than normal. In some pregnancies, the body fails to make enough insulin, and GD may develop.

What is insulin?

Insulin is essential hormone that plays a key role in your glucose metabolism. It is produced by pancreas. With insulin, glucose in the blood can be effectively absorbed by cells of the body for energy. And if there something goes awry with insulin, the body will lose its natural ability to regulate the balance of glucose in the blood.

When pregnancy is over, so is gestational diabetes. Soon after delivery, the pregnancy hormones and placenta go away. Then insulin will return to normal.

Doctors don’t know why some pregnancies develop GD. But in general, the risk of developing the condition is high in women with the following risk factors:

  1. Being obese before pregnant.
  2. Having pre-diabetes before pregnant, a condition in which you have high blood sugar but not high enough to be categorized into diabetes. See also the table of normal and abnormal blood sugar levels!
  3. GD is also likely to run in families. If you have a family history of GD or diabetes mellitus, your risk is higher to develop the same condition.
  4. A personal history of GD. If you have had GD in your previous pregnancy, you’re likely to have it again in your next pregnancy.
  5. GD is relatively more common in Native American, African-American, Hispanic, and Asian.

What happen if gestational diabetes is poorly controlled?

Again, GD doesn’t go away during pregnancy. But this doesn’t mean that you can ignore it. It’s always important to make sure that your GD is well controlled.

Poorly-controlled high blood sugar will pay the price in some consequences. The following are some complications that may occur if your GD is poorly controlled:

  1. The risk of a serious pregnancy complication called preeclampsia, typically characterized by excessive protein in the urine and high blood pressure. It can hurt both the mother and baby – even sometime it could cause death. It is commonly found during the second half of pregnancy, though sometime it may also develop earlier.
  2. The risk of giving birth earlier than normal due to the baby has grown too big or if you have preeclampsia or due to other reasons. And you may need to take a cesarean section (c-section) to deliver baby earlier.
  3. And premature birth also carries some consequences. The baby is not only at high risk of getting overweight (larger than normal) at birth, but also may experience hypoglycemia (low blood glucose) right after birth, respiratory distress syndrome (a breathing problem), and a greater chance of dying soon after or before birth.

GD also increases the risk of type-2 diabetes. All of these risks may make you worry about your pregnancy. But these risks are so preventable. Even many pregnant women with GD, especially if the condition is well controlled, have normal pregnancies and deliver healthy babies.

Gestational diabetes fasting blood sugar targets

Your doctor usually asks you to check blood glucose at certain times of day, particularly such as after fasting or before your first meal of the day. As the name implies, fasting means refraining from eating or drinking (except plain water).

Fasting blood sugar is used for a number of reasons. It can be used to see how well your blood sugar is controlled. It may also help analyze the effectiveness of diabetic treatment you’re taking.

Again, fasting blood sugar 105 and 110 are still considered high in GD. The blood sugar level targets may vary from woman to woman – ask your healthcare provider for more advice. In general, the following are recommended blood sugar targets for pregnant women with GD:

Fasting blood glucose levels and initiation of insulin therapy in gestational diabetes


To determine whether an initial fasting blood glucose determination will predict which pregnant women will need insulin in addition to dietary measures to maintain fasting glucose levels during gestation.


All women referred for management of gestational diabetes received dietary counseling and instructions for self-monitoring of blood glucose levels during fasting and at 2 hours after each meal. Insulin therapy was initiated if the fasting blood glucose value exceeded 5.8 mmol/L (105 mg/dL) on more than one occasion, the 2-hour postprandial glucose exceeded 8.3 mmol/L (150 mg/dL), or the 2-hour postprandial glucose exceeded 6.7 mmol/L (120 mg/dL) three times in a week. The use of diet alone or diet plus insulin therapy was determined by review of medical records.


Fifty-two pregnant women with fasting blood glucose levels of less than 5.8 mmol/L (105 mg/dL) and with two or more elevated blood glucose values on a 3-hour glucose tolerance test underwent follow-up at least through the 36th week of gestation. In 21 patients, insulin therapy was initiated in addition to diet. Two of five women with an initial fasting glucose level of less than 4.4 mmol/L (80 mg/dL) required insulin, and 8 of 24 women with fasting levels of 5.3 to 5.8 mmol/L (96 to 105 mg/dL) eventually needed insulin.


The height of the fasting blood glucose level in women with gestational diabetes does not separate those who will maintain blood glucose levels in the targeted therapeutic range on diet alone from those who will need insulin. Therefore, all women with gestational diabetes need to participate in self-monitoring of blood glucose levels.

Blood sugar 105 mg/dl fasting – good or bad?

We help you interpret your blood sugar values. You have tested your blood sugar fasting and the result was 105 mg/dl. The corresponding A1C is 5.3%. Let’s have a look at the blood sugar gauge:

Your result is:

Slightly too high blood sugar (beginning hyperglycemia)

To improve your blood sugar fasting you need to
lower your blood glucose level by 5mg/dl.

Your fasting blood sugar level should always be below 100mg/dl but not fall below 80mg/dl.

Blood sugar testing measures how much glucose is in the bloodstream. No matter what is eaten, from a small snack to a large meal, blood glucose values rise in response to any carbohydrates that are digested.Check your fasting blood sugar

In a healthy person, the pancreas reacts to the higher blood glucose by releasing insulin, a hormone that converts blood sugar into usable energy.

In addition to carbohydrates, other body processes also raise blood sugar levels.When a person fasts, which is defined medically as not eating or drinking anything aside from water for at least eight hours, the release of glucagon is triggered in the body. Glucagon instructs the liver to metabolize reserve supplies of glycogen, which are then circulated into the bloodstream as sugars. Accordingly, the amount of plasma glucose goes up. This is how the body creates energy even while fasting.

In sum, when diabetes is not present the body responds to all blood sugars by manufacturing insulin in proportion with the glucose level. When it comes to fasting blood sugars, insulin lowers and stabilizes the levels so that they remain in a normal, healthy range. Yet when any form of diabetes is present, either pre-diabetes, Type 1 diabetes or Type 2 diabetes, the whole physiological process doesn’t work correctly, and blood sugars are often considerably higher than normal. The fasting blood sugar test (FBS) is commonly used to detect the existence of diabetes.

In order to prepare for a fasting blood sugar test, one must refrain from eating or drinking from eight to twelve hours before the test, depending upon the doctor’s instructions. It is conducted in the same manner as any laboratory blood test. The health professional will wrap an elastic band around the upper arm in order to restrict blood flow, which enlarges the veins and facilitates the insertion of a needle. After disinfecting the site with alcohol, a needle is placed into the vein and blood is drawn into a vial, which will be then be sent for laboratory testing.

Intermittent fasting diet

A normal result for fasting blood glucose ranges from 70 – 100 mg/dL. According to criteria set by the American Diabetes Association, a higher than normal fasting blood sugar between 100 to 125 mg/dL (5.6 to 6.9 mmol/L) may indicate prediabetes. This shows an increased risk of developing Type 2 diabetes.

When the measurement is above 126 mg/dL (7 mmol/L), a diagnosis of diabetes is likely. A lower than normal result may point to hypoglycemia that is caused by a specific type of tumor in the pancreas, and further diagnostic testing is needed.

Besides eating or drinking during the eight hours before the fasting blood sugar test, other factors may influence the outcome. Illness, drinking alcohol or excessive caffeine the day before, smoking and emotional stress can all impact blood sugar levels. Fasting blood sugar tests should therefore be performed twice, on two separate days, in order to confirm that results are consistent.

Non-Fasting Glucose: What Are Normal Blood Sugar Levels?

People with diabetes should test their non-fasting glucose levels regularly.

Image Credit: PeopleImages/E+/GettyImages

Non-fasting glucose levels can be a key measurement of any person’s health, and regular blood sugar testing is an especially critical part of any diabetes care plan.

Here’s what you should know about non-fasting blood work, including normal blood glucose levels.

Glucose 101

Blood sugar, or glucose, is one of the body’s primary sources of fuel, which it mainly gets by metabolizing the carbohydrates in food. The hormone insulin helps move glucose out of the blood and into the cells.

But people with diabetes either don’t make enough insulin or can’t use the insulin their bodies do make effectively, according to the American Diabetes Association (ADA). This results in high blood sugar, or hyperglycemia. People with diabetes can also experience low blood sugar (hypoglycemia), especially if they are taking blood sugar-lowering medications like insulin.

A blood sugar level is simply a measurement of how much glucose is in the bloodstream at the moment you check. If you have diabetes, your doctor will help you determine how frequently you need to check your sugar level. According to the Mayo Clinic, people with diabetes may need to monitor their blood sugar anywhere from two to 10 times per day.

What Is Normal Non-Fasting Glucose?

Normal non-fasting blood sugar levels should be less than 180 milligrams per deciliter (mg/dL) for those with diabetes, according to the ADA. For those without diabetes, it’s less than 140 mg/dL, according to Virginia Mason Diabetes Care.

Blood Sugar Before and After Meals

There are many different times of day when you can check your blood sugar, but the most important times are typically before and after a meal. Checking your blood sugar before a meal can help you decide which foods to eat and how much insulin to take. According to the ADA’s Standards of Medical Care in Diabetes — 2019, a healthy blood sugar level before a meal should fall somewhere between 80 and 130 mg/dL.

Checking your blood sugar after you eat tells you how your body is processing your meal and whether or not you currently have enough insulin in your system. But don’t check your blood sugar immediately after you finish your food. “If a patient wants to see their body’s response to a meal, they need to wait two hours before checking blood glucose,” says Samar Hafida, MD, an endocrinologist at Boston’s Joslin Diabetes Center. “That’s how long it takes for the body to fully digest carbs.”

To see the effect of a meal on your blood glucose, measure your blood sugar two hours after starting your meal; that’s when your blood sugar will peak. According to the ADA, the goal is that this peak, non-fasting glucose level will be less than 180 mg/dL.

Read more: How Long Does It Take for Blood Sugar Levels to Peak After Eating?

Your blood sugar levels will measure differently before and after meals.

Image Credit: Marco_Piunti/iStock/GettyImages

Blood Sugar Levels at Night

It’s also important to check your blood sugar before bedtime. According to the Joslin Diabetes Center, your before-bed blood sugar should be between 90 and 150 mg/dL. If your level is lower than this, you may need to have a small snack to prevent your blood sugar from falling too low overnight.

If you notice that your morning blood sugar levels are high, it may be due to something called the Somogyi effect, according to the Cleveland Clinic. This phenomenon occurs when blood sugar levels drop too low overnight, prompting the liver to release stored glucose to “rescue” you. If your doctor suspects that you are experiencing the Somogyi effect, he or she may ask you to check your blood sugar between 2 and 3 a.m. for several nights in a row. If your overnight sugars are indeed too low, your doctor will help you come up with a plan to manage the situation.

Read more: How to Quickly Reverse a Sugar Crash

When Should You Check Your Non-Fasting Glucose Levels?

Talk with your doctor about how often you need to check your blood sugar. Testing will depend on the type of diabetes medicine you take, as well as your overall glucose level (aka A1C level). If you’re new to insulin, you’ll likely have to check your blood sugar several times a day. Other people with diabetes may only need to check their levels a few times a week.

You might occasionally need to check your blood sugar at times unrelated to a meal or bedtime. For example, if your doctor has recently made a change to your diabetes medication, he or she may ask you to monitor your blood glucose more frequently throughout the day in order to gauge how well your new medications are working.

You may also experience elevated blood sugars when you’re sick, as this can be part of the body’s natural response to fighting an infection, according to the National Institutes of Health. If you have a cold, therefore, you might need to check your blood sugar levels more frequently. Blood glucose can also be elevated during pregnancy or times of stress.

If you experience the symptoms of hypoglycemia, check your blood sugar ASAP. This is the only way to actually confirm that it’s low, according to the ADA.

It’s not a good idea to check your blood sugar without a clear reason, however. “The meaningful data points provided by blood sugar readings are usually tied to a meal,” Dr. Hafida explains. Checking blood sugar randomly — especially directly after a meal — can be misleading, and might cause you to adjust your medicine or carb intake incorrectly.

School of Diabetes – Self-Monitoring of Blood Glucose

The main goal of treatment is to achieve normal or near-normal glycated hemoglobin levels (reflects the “average” blood glucose levels over 2-3 months) to prevent complications of diabetes.

The individual goal of treatment (glycated hemoglobin and fasting glucose level) you choose together with your doctor, it will depend on several conditions: the duration of the disease and the presence of complications, age and concomitant diseases, etc.d.

In most cases, the optimal target is a glycated hemoglobin level <7%. In order to achieve this goal, it is necessary that the blood glucose level during self-monitoring does not exceed the corresponding values ​​(see table below).

Individual treatment goals for fasting / pre-meal plasma glucose and 2 hours post-meal depending on the selected target glycated hemoglobin (HbA1c) level.

HbA1c,% Plasma glucose on an empty stomach / before meals, mmol / l Plasma glucose 2 hours after meals, mmol / l
<6.5 <6.5 <8.0
<7.0 <7.0 <9.0
<7.5 <7.5 <10.0
<8.0 <8.0 <11.0

For self-monitoring of blood glucose, use:

Test strips for portable devices – glucometers.The use of the meter does not require special training, it is only necessary, as before using any household appliance or equipment, to carefully read the instructions. Glucometers differ among themselves primarily by the method of the test (electro- and photochemical), as well as the speed of determination (from 5 to 45 seconds), the presence or absence of a special code, the memory size of the results and other functions. The technique is very simple: you need to turn on the device, enter the code of the test strips (if necessary), insert the test strip and apply on it a small drop of blood obtained from the finger (the test strip with a capillary device will suck blood from the drop by itself).

See more Technique for taking a drop of blood.

Modern glucometers allow you to quickly get an accurate result (permissible error of 10-20%) anywhere (you can carry them with you), and also have a number of useful additional functions, the number of which is constantly increasing (memory, sound signal for visually impaired patients, the possibility download results to a computer, etc.)

At the same time, it is necessary to take into account your possibilities: choose a device that you can afford to “maintain”, since the main expenses are not the cost of the device, but the cost of consumables – test strips.Sometimes the costs of purchasing test strips can be partially covered by relatives, for example, as a gift for a holiday, you can ask for a gift of test strips.

Remember that you need to calibrate your meters on a regular basis (check their accuracy with a known concentration of glucose solution supplied with the meter, or in laboratories / firms that offer such services), and change the batteries in time.

Remember not to use

test strips

  • Exposed to high or low temperatures
  • Expired

  • Stored in an open box

How often should self-monitoring of blood glucose be performed?

General rules for self-testing are approximately as follows.

In everyday life, for patients on insulin, self-monitoring of blood glucose levels should be performed daily at least 4 times a day – before meals and before bedtime, sometimes 2 hours after meals, and several times a month at 2-4 am.

The frequency of self-monitoring of blood glucose levels depends on the type of antihyperglycemic therapy:

Type of hypoglycemic therapy Frequency of examination
On intensive insulin therapy At least 4 times daily
On oral glucose-lowering therapy and / or GLP-1 receptor agonists and / or basal insulin At least 1 time per day at different times + 1 glycemic profile (at least 4 times a day) per week
On ready-mixed insulin At least 2 times a day at different times + 1 glycemic profile (at least 4 times a day) per week
On diet therapy Once a week at different times of the day

Additional measurements will be required in the following situations:

  • sports
  • travel
  • symptoms of hypoglycemia
  • before driving.

Regular blood glucose measurements allow the trained patient to independently adjust their insulin doses and / or adjust their diet and physical activity to achieve target blood glucose values ​​to prevent future complications. However, sometimes self-monitoring blood glucose data are insufficient to understand the causes of poor glycemic control. Installing a continuous blood glucose monitoring system (CGMS) can help in this situation.

90,000 Clinical Study Fasting Glucose Disorder: 25% Fiber, 0% Fiber – Clinical Trials Registry
Secondary Findings







Measure Time limit
Cmax for glucose in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
AUC for glucose in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Tmax for glucose in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Cmax for triglyceride in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
AUC for triglycerides in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Tmax for triglycerides in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Cmax for RLP cholesterol in IFG Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
AUC for RLP cholesterol in IFG Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
RLP cholesterol Tmax in IFG Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Cmax for RLP cholesterol in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
AUC for RLP cholesterol in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
RLP cholesterol Tmax in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Insulin Cmax for IFG Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Insulin AUC for IFG Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Insulin Tmax for IFG Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Cmax for insulin in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
AUC for insulin in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.
Tmax for insulin in healthy, overweight participants Blood samples will be taken in -35, 10, 20, 30, 40, 50, 60, 75, 90, 105, 120, 150, 180, 210 and 240 minutes.

Correlation between blood pressure variability and blood glucose level in arterial hypertension and type 2 diabetes mellitus

1. Abusuev SA, Gadzhiev GE. Arterial, hypertension in patients with diabetes mellitus and its treatment. – Makhachkala: DSMA, 1996; 27.

2. Ageev F.T., Fomin IV ‘., Mareev V.Yu., Belenkov Yu.I. Prevalence of arterial hypertension in the European part of the Russian Federation: Data from the EPHA study, 2003 // Cardiology 2004; 11: 50-51.

3. Alisheva E.K., Krasilnikova E.I., Shlyakhto E.V. Methods for the diagnosis of insulin resistance // Arterial. hypertension 2002; 8 (1): 23-32.

4. Almazov V.A., Blagosklonnaya Ya.V., Shlyakhto E.V .:, Krasilnikova E.I. Metabolic cardiovascular syndrome. S / Pb .: SPbGMU, 1999; 204.

5. Almazov V.A., Shlyakhto E., Sokolova L.A. Borderline arterial hypertension. – S / Pb .: Hippocrates, 1992; 186.

6. Almazov V.A., Shlyakhto E.V. Academician G.F. Lang and his school. M .: Medicine, 1999: 28-42.

7. Diamonds. V.A., Shlyakhto E.V., Krasilnikova E.I. and other Violation of immunological parameters in patients with insulin resistance syndrome // Cardioology 2001; 8: 54-58.

8. Ametov A.G., Gubina E.V., Nikolaev O.G. The effectiveness of berlipril in patients with non-insulin dependent diabetes mellitus with mild and moderate arterial hypertension according to 24-hour blood pressure monitoring // Ter.archive 1999; 8: 17-23.

9. Ametov A.C. Insulin secretion and insulin resistance: two sides of the same coin // Probl. endocrinol. 2002; 3: 31-37.

10. Ametov A.S., Granovskaya-Tsvetkovaya A.M., Kazei N.S. Non-insulin dependent diabetes mellitus. Fundamentals of pathogenesis and therapy. M .: MIA, 1995; 64.

11. Ametov A.S., Demidova T.Yu. ‘, Smagin L.V. Prospects for the effect of antihypertensive therapy on the pathogenetic mechanisms of insulin resistance syndrome // Probl. endocrinol. 2005; 1: 34-40.

12. Ametov A.S., Demidova T.Yu., Smagii JI.B. Combined pharmacotherapy of arterial hypertension in patients with type 2 diabetes mellitus // Arterial. hypertension 2004; 10: 16-26.

13. Baevsky R.M., Berseneva A.P. Assessment of the body’s adaptive capabilities and the risk of developing diseases. M .: Medicine, 1997; 265.

14. Baevsky R.M., Ivanov G.G. Heart rate variability: theoretical aspects and possibilities of clinical application // Ultrasound and functional.diagnostics 2001; 3: 108-127.

15. Bakshiev * V.I., Kolomoets N.M. Self-monitoring of blood pressure on an outpatient basis // Klin. honey. 2002; .8; 9-13.

16. Balabolkin M.I. Diabetes. -M .: Medicine, 1994; 365.

17. Balabolkin M.I., Klebanova E.M., Kreminskaya V.M. Pathogenesis and mechanisms of development of angiopathies in diabetes mellitus // Cardiology 2000; 10: 74-87.

18. Balabolkin M.I., Kreminskaya V.M. Are new diagnostic criteria and classification of diabetes mellitus necessary? // Probl.endocrinol. 1999; 3: 21-25.

19. Balabolkin M.I., Kreminskaya V.M. Pathogenesis and prevention of vascular complications of diabetes mellitus. // Ter. archive 1999; 10: 5-12.

20. Balabolkin M.I., Kreminskaya V.M., Klebanova E.M. The role of endothelial dysfunction and oxidative stress in the mechanism of angiopathy development in type 2 diabetes mellitus // Cardiology 2004; 7: 90-93.

21. Belousov Yu.B., Leonova M.V. Clinical efficacy of the new beta-blocker nebivolol in patients with arterial hypertension (results of a multicenter study) // Cardiology 2000; 9: 27-33.

22. Bogdanovich B.JI. Diabetes mellitus (treatment and prevention). N. Novgorod: NGMA, 1998; 192.

23. Boytsov S.A. New Russian guidelines for the prevention, diagnosis and treatment of arterial hypertension: what’s new in them? // Arterial. hypertension 2005; 5: 33 -46.

24. Borovikov V: P. A popular introduction to 8TAT18T1CA. M .: Computer Press, 1998; 267.

25. Borovkov N.I .:, Sidorova N.V. Interrelation of indicators of the daily profile of blood pressure and heart rate variability in patients with arterial hypertension with non-insulin dependent diabetes mellitus // Klin.honey. 2002; 7: 19-21.

26. Burtsev V.I. Topical issues of arterial hypertension in clinical medicine // Klin. honey. 2005; eight; 25-31.

27. Bakris D., Sowers D., Epstein M., Williams M. Hypertension in diabetic patients: why is active management so important? // International honey. magazine 2000; 5: 16-19.

28. Vorobiev K.P. Clinical and physiological analysis of the categories of the functional state of the body and intensive “therapy // Bulletin of intensive therapy 2001; 2: 3-8.

29.Voskresensky A.D., Wentzel M.D. Statistical analysis of heart rate and hemodynamic parameters in physiological studies. Moscow: Nauka, 1974; 221.

30. Ginzburg M.M., Kozupitsa G.S. Insulin resistance syndrome // Probl. endocrinol. 1997; 1: 40-43.

31. Ginzburg M.M., Kozupitsa G.S., Sergeev O.V. Insulin content and blood pressure in obese women // Probl. endocrinol. 1996; 4: 17-19.

32. Ginzburg M.M., Sergeev O.V., Kozupitsa G.S. Dependence of blood pressure on the distribution of fat in obese women // Probl.endocrinol. 1997; 1: 22-25.

33. V.E. Gmurman. Theory of Probability and Mathematical Statistics. M .: Higher school, 2001; 478.

34. Gorbunov V.M. 24-hour automatic blood pressure monitoring (recommendations for doctors) // Cardiology 1997; 6: 96-104.

35. Gorbunov V.M. The value of studying various types of blood pressure variability in patients with arterial hypertension // Cardiology 1997; 1: 66-69.

36.Dedov I.I., Shestakova M.B. Diabetes mellitus and arterial hypertension. -M.: MIA, 2006; 343.

37. Dedov I.I., Suntsov Yu.I., Kudryakova S.B., Ryzhkova S.G. Epidemiology of insulin-dependent diabetes mellitus // Probl. endocrinol. 1998; 2: 47-51.

38. Dedov I.I., Suntsov Yu.I., Kudryakova S.B., Ryzhkova S.G. Epidemiology of non-insulin dependent diabetes mellitus // Probl. endocrine. 1998; 3: 45-48.

39. Demin A.A. Modern principles of treatment of arterial hypertension // Klin. honey. 2003; 5: 4-9.

40.Didenko V.A. Metabolic syndrome X: history and etiopathogenesis // Lab. honey. 1999; 2: 49-57.

41. Tree A.B. Treatment of uncomplicated non-insulin dependent diabetes mellitus // Probl. endocrinol. 1995; 4: 27-34.

42. Dreval A.B., Misnikova I.V., ‘Redkin Yu.A. and other Epidemiological examination of the population of patients with NIDDM in the regions of the Moscow region (based on a computer register) // Probl. endocrinol. 1999; 3: 3-7.

43. Dreval A.B., Rimanchuk G.V., Loseva V.A., Redkin Yu. A. Prevalence of diabetes mellitus in children and adolescents of the Moscow region // Probl. endocrinol. 1997; 2: 3-5.

44. European Society of Hypertension. European Society of Cardiology 2003. Recommendations for the diagnosis and treatment of arterial hypertension // Arterial. hypertension 2004; 3: app .; 63.

45. Zhuplatov S.B., Trusov V.V. Features of cardiohemodynamics in diabetes mellitus // Probl. endocrinol. 1995; 2: 6-8 ‘.

46. Zyugdzha A.Yu., Staponkene M.A., Pyatkavichene R.I., Bauyavichus E.V. Arterial, hypertension: prevalence, priority areas of prevention // Ter. archive 1992; 1: 66-70.

47. Zavyalov A.B. The ratio of body functions. -M .: Medicine, 1990: 12-30.

48. Zadionchenko B.C., Adasheva T.V., Sandomirskaya A.P. and <- other. Influence of nebivolol on the daily blood pressure profile and morphofunctional parameters of the heart in patients with mild and moderate arterial hypertension // Cardiology 2000; 7: 12-15.

49. Zaitsev V.M., Liflyandsky V.G., Marinksht V.I. Applied Medical Statistics. – SPb: Foliant, 2003; 432.

50. Yu.V. Zimin Insulin resistance, hyperinsulinemia and arterial hypertension // Cardiology 1996; 11: 80-88.

51. Yu.V. Zimin Origin, diagnostic concept and clinical significance of insulin resistance syndrome or metabolic syndrome – “X” // Cardiology 1998; 6: 71-81.

52. Yu.V. Zimin Clinical and hemodynamic characteristics of hypertension associated with insulin resistance // Cardiology 1998; 9: 98-103.

53. Ismailov S.I., Yafasov K.M., Sirozhiddinova N.Z. Therapy of arterial hypertension in patients with type 2 diabetes mellitus // Probl. endocrinol. 2003; 2: 17-23.

54. Kabalava Zh.D., Kotovskaya Yu.V., Tereshchenko S.N., Moiseev V.C. Clinical i value of 24-hour blood pressure monitoring for selection; tactics of treatment of patients with arterial hypertension // Cardiology 1997; nine: ! “;. 98-103. • ” ■ •”.

55. Kabalava Zh.D., Kotovskaya Yu.V. Blood pressure monitoring: methodological aspects of the clinical significance / Ed.Q: S. Moiseeva; -M .: Servier, 1999; 234.. ‘■■■ V’.

56. Kamysheva1 E.P. Cardiac ischemia. and diabetes // 5 Cardiology 1994; 7: 23-25. ”

57. Kamysheva E.P .:, Pokalev G.M. Diabetes mellitus (modern | ‘concept, clinical symptoms, syndroms and medical; tactics): H;

58. Novgorod: NGMA; 1999; 142.gf 63. Kassenova C.J1. Vasopressin and the renin-aldosterone system in patients with arterial hypertension // Clin. honey. 2002; 12: 31-33.1 ‘•’ ” ‘■’ ” ■ ‘

59.Komarov F.I., Rapoport S.I., Malinovskaya N.K. Circadian rhythms in the clinic of internal diseases // Klin. honey. 2005; 8: 8-12.

60. Kondrat’ev Ya.Yu., Nosikov V.V., Dedov I.I. Polymorphic genetic markers and vascular complications of diabetes mellitus // Probl. endocrinol. 1998; 1: 43-51.

61. Konstantinov V.V., Zhukovsky G.I., Timofeeva T.N. et al. Prevalence of arterial hypertension and its relationship with mortality and risk factors among the male population in cities of different regions // Cardiology 2001; 4: 39-41.

62. Kotova JI.H., Goloshchapov O.A. Some indicators of central and pulmonary hemodynamics in patients with diabetes // Blood circulation 1987; 2: 53-55.

63. Kotovskaya Yu.V., Kabalava Zh.D., Lobankova JI.A., Tolkacheva V.V. Disproportionality of the daily rhythm of blood pressure in patients with arterial hypertension and type 2 diabetes mellitus // Arterialn. hypertension 2003; 2: 18-36.

64. Krasnoshchekov S.P., Petrov A.A. Principles of building models. Moscow: Moscow State University, 1983; 246.

65. Kudryakova S.B., Suntsov Yu.I., Ryzhkova S.G. Prevalence of complications of diabetes mellitus according to the register // Probl. endocrinol. 1995; 4: 8-11.

66. Kudryakova S.B., Suntsov Yu.I., Nechaeva I.S. and other Dynamics of epidemiological indicators of diabetes mellitus in the central administrative district of Moscow according to the state register // Probl. endocrinol. 2001; 4: 14-17.

67. Kuzin A.I., Cherednikova M.A., Vasiliev A.A., Kamerer O.V. Arterial hypertension and type 2 diabetes mellitus in patients with metabolic syndrome: features of the effect on the lipid spectrum // Arterial.hypertension 2003; 2: 36-42.

68. Kuraeva T.L., Remizov O.V., Dedov I.I. Medico-genetic counseling and predicting the development of insulin-dependent diabetes mellitus // Probl. endocrinol. 1996; 6: 46 49.

69. Kurdanov Kh.A., Medalieva R.Kh., Huranova L.M., Barasbieva G.I., Polesskiy V.A. Ischemic heart disease and

70. Kushnakovsky M.S. Hypertonic disease. Saint Petersburg: Sotis, 1995; 316.

71. Lebedev N.B., Yazdovsky V.V., Shcherbacheva L.N. and other Complications of type I diabetes mellitus and antigens of the HLA system // Probl. endocrinol. 1995; 5: 4-7.

72. Leonova M.V., Belousov Yu.B., Semenchuk G.A. and other Analysis of indicators of ambulatory monitoring of blood pressure in patients with arterial hypertension // Ter. archive 1997; 1: 35-38.

73. Mazovetskiy A.G., Velikanov V.K. Diabetes. M .: Medicine, 1987; 284.

74. Makolkin V.I., Podzolkov V.I., Gilyarov M.Yu. Possibilities of daily monitoring of blood pressure in the differential diagnosis of neurocircular dystonia and hypertension // Cardiology 1997; 6: 24-28.

75. Mamedov M.N., Perova N.V., Metelskaya V.A., Oganov R.G. The relationship of abdominal obesity and insulin resistance syndrome in patients with arterial hypertension // Cardiology 1999; 9: 18-22.

76. Mamedov M.N., Metelskaya, V.A., Perova N.V. Metabolic syndrome: ways of realizing atherothrombogenic potential // Cardiology 2000; 2: 83-89.

77. Mamedov M.N. Glucose Tolerance: Who Should Treat and How? // Cardiovascular Therapy and Prevention 2005; 6 (p.1): 89-96.

78. Mamedov M.N., Oganov R.G. Epidemiological aspects of metabolic syndrome // Cardiology 2004; 9: 1-4.

79. Martynov A.I., Ostroumova O.D., Mamaev V.I., Rybkina T.E., Novinsky A.A., Melnikov O.A. Variability of blood pressure in arterial hypertension and the effect of antihypertensive therapy // Klin, med. 2002; 6: 4-7.

80. Macheret E.L., Murashko N.K., Chaban T.I. Heart rate variability depending on the type of vegetative dystonia syndrome course // Bulletin of arrhythmology 2000; 16: 17-20.

81. Melnichesnko G.A., Pyshkina E.A. Obesity and insulin resistance – risk factors and a component of metabolic syndrome // Ter. archive 2001; 12: 5-8.

82. Mingazetdinova L.N., Mutalova E.G., Kanevskaya. N.P., Absalyamova Yu.R. Arterial hypertension with metabolic syndrome: effect on the platelet-vascular link of hemostasis // Arterial. hypertension 2004; 4: 18-24.

83. L.V. Nedosugova New approaches to the therapy of diabetes mellitus // Russian med. magazine 2006, 13: 17-22.

84. Nikitin Yu.P., Kazeka G.R., Simonova G.Yu. Prevalence of the components of the metabolic syndrome “X” in the disorganized urban population (epidemiologist, research) // Cardiology 2001; 9: 37-40.

85. Nikolaev A.Ya. Biological chemistry. M .: MIA, 1998; 496.

86. Nash D. Diabetes mellitus and cardiovascular diseases // Intern. honey. magazine 2002; 6: 17-23.

87. Oganov R.G. The problem of controlling arterial hypertension among the population // Cardiology 1994; 3: 80-83.

88. Oganov R.G. Epidemiology of arterial hypertension in Russia and the possibilities of prevention // Ter. archive 1997; 69: 3-6.

89. Oganov R.G. Preventive cardiology: from hypotheses to practice // Cardiology 1999; 2: 4-9.

90. Oganov R.G. Prevention, diagnosis and treatment of primary arterial hypertension in the Russian Federation // Klin. farm. and rub. 2000; 3: 5-30.

91. Oganov RG, Nebieridze, DV: Strategy for optimal blood pressure control: the place of fixed low-dose combinations // Cardiovascular therapy and prevention 2000; 1-2: 72-79.hypertension // Ter. archive 1994; eight; 70-73.

93. Shaleev N.R., Kalinin A.P., Mravyan S.R. Diabetes mellitus and heart // Klin, honey. 2005; 8: 37-41.

94. Panin JI.E. Biochemical mechanisms of stress: – Novosibirsk: Nauka, 1983; 216.

95. Petrova T.V., Stryuk R.I., Bobrovnitsky., I.P. • et al. On the relationship of excess body weight, arterial hypertension, hyperinsulinemia and impaired glucose tolerance // Cardiology 2000; 2: 30-34.

96. Podpalov V.P., Deev A.D., Sivakov V.P., Rozum JI.A. Predictive value of heart rate variability parameters as a risk factor for the development of arterial hypertension // Cardiology 2006; 1: 39-42.

97. I. V. Samorodskaya Cardiovascular morbidity and risk factors for cardiovascular events in the Russian Federation // Cardiovascular Therapy and Prevention 2005; 3 (part 2): 94-100.

98. Selye G. At the level of the whole organism. Moscow: Nauka, 1972; 121.

99.Sidorenko B.A., Preobrazhensky D.V., Romanova N.E. Hypertension in old age: prevalence, clinical significance, and drug therapy // Cardiology 1999; 12: 71-76.

100. P. I. Sidorov, A. G. Soloviev, M. N. Pankov. and other Features of the course of diabetes mellitus in alcohol abuse // Probl. endocrinol. 1999; 6: 10-13.

101. Silnitsky P.A. Diabetes mellitus and myocardial infarction // Probl. endocrinol. 1997; 4: 117- 122.

102. Smirnova O.M. The role of combination therapy in the treatment of type 2 diabetes mellitus // Consilium medicum 2005; 07 (9): 8- 16:

103.Sobetsky B.B. Reflexology in clinical practice. Kiev: Health, 1993; 144.

104. Sobolev A.B., Lyutikova L.N., Ryabykina G.V., Aleeva M.K., Mareev V.Yu. Rhythmogram variation as a new method for assessing heart rate variability // Cardiology 1996; 4; 47-52.

105. Sokolov E.I. Damage to the myocardium and blood vessels in diabetes mellitus // Ter. archive 2001; 12: 9-13.

106. Sokolov E.I. Diabetes mellitus and atherosclerosis. Moscow: Nauka, 1996; 404.

107.Sowers J.R., Lester M. A. Diabetes and cardiovascular diseases // Intern. honey. magazine 1999; 11-12: 21-26.

108. Strogin L.G., Pochinka I.G. Features of chronic heart failure in patients with type 2 diabetes mellitus // Cardiology 2005; 2: 33-36.

109. Suntsov Yu.I., Zhukovsky G.S., Mazovetsky A.G. and others. The value of the level of insulinemia in the prevalence of dyslipoproteinia and coronary heart disease in men 20-69 years old // Cardiology 1984; 24: 36-39.

110.Surkova E.V., Antsiferov M.B. The role of training programs in the treatment of patients with type II diabetes mellitus // Probl. endocrinol. 1995; 6: 4 6.

111. Taton Jan. Obesity. Pathophysiology, diagnosis, treatment: Per. from Polish A. Gasperovich. Warsaw: Polsk. honey. publ., 1981; 363.

112. Telkova I.L., Teplyakov A.G., Karpov P.C. Hyperinsulinemia and its contribution to the clinical course and outcomes of myocardial infarction. Data of 5-year prospective observation // Ter. archive 2002; 9: 20-25.

113. Fomin I.B. Arterial hypertension in the Russian Federation for the last ten years. What’s next? // Heart 2007; 6: 120-122.

114. Khadapash L.A., Perova I.V., Mamedov M.N., Olfer’ev A.M., Metelskaya V.A., Melkina O.N., Oganov R.G. Clusters of metabolic syndrome components in patients with type 2 diabetes mellitus // Probl. endocrinol. 2001; 4: 30-34.

115. Chazov V.I. Diagnostics in the XXI century: from subjective to objective // ​​Ter. archive 2001; 8: 5-8.

116. Chazova L.V., Kalinina A.M., Markova E.V., Pavlova L.I. Diabetes mellitus: prevalence, relationship with risk factors for coronary artery disease, prognostic value (epidemiological study) // Ter. archive 1996; 3: 15-18.

117. Chazova I.E., Mychka V.B. Metabolic syndrome and arterial • hypertension // Arterial. hypertension 2002; 1: 17-24.

118. Chazova I.E. Is it possible to prevent the development of type 2 diabetes mellitus (results of the Stop-NDDM study) // Arterialn. hypertension 2003; 3: 15-20.

119.IZ Shalnova S.A., Deev A.D., Oganov G.V. Factors affecting mortality from cardiovascular diseases in the Russian population // Cardiovascular therapy and prevention 2005; 1: 4-9.

120. Shamkhalova M.Sh., Chugunova L.A., Shestakova M.V. Diabetes mellitus and its complications: new possibilities of insulin therapy for type 2 diabetes mellitus // Consilium.medicum 2005; 9: 11-17

121. Sharafetdinov Kh.Kh., Meshcheryakova V.A., Plotnikova O.I., Maltsev G.Yu., Petel E.P. Influence of food loads on glycemia, levels of insulin, C-peptide, and gastrointestinal inhibitory polypeptide in patients with type II diabetes mellitus // Probl.endocrine. 1999; 6: 6-9.

122. Shestakova M.V. The problem of arterial hypertension in diabetes mellitus // Cardiology 1999; 6: 59-65.

123. Shestakova M.V. Elimination of insulin resistance is the basis for the treatment and prevention of type 2 diabetes mellitus // Russian med. zhurn. 2004; 12: 16-22.

124. Shlyakhto E.V., Konradi A.O. Causes and consequences of activation of the sympathetic nervous system, with arterial hypertension // Arterial. hypertension. 2003; 3: 81-87.

125. Shlyakhto E.V., Konradi A.O. Classification of arterial hypertension: from Bright’s disease to the cardiovascular continuum // Arterial. hypertension 2004; 2: 12 -24.

126. Shulutko B.I. Hypertension, illness and other forms of arterial hypertension. S / Pb .: Renkor, 1998; 200.

127. Shustov G.B., Romashevsky B.V. Influence of glurenorm on the level of blood pressure in patients with non-insulin dependent diabetes mellitus with essential hypertension // Probl. endocrinol. 1998; 1: 15-19.

128.Shutepova E.I., Nazarova O.A., Gridnev V.V., Barochkina O.Yu. Arterial hypertension in elderly patients in the practice of physicians in the Ivanovo region // Klin. honey. 2004; 3: 67-71.

129. NZ Elbaev A.D., Kurdanov Kh.A. Diabetes mellitus and arterial hypertension: mechanisms of interrelation and ways of correction. – M: Ileksa, 2003; 136.

130. Elgarov A.A., Inarokova A.M. The effectiveness of the program * for the prevention of arterial hypertension among the organized population // Ter. archive 1992; 1: 16-19.

131. Emanuel Yu.V., Karyagina I.Yu. Laboratory technologies for diagnosis and monitoring of diabetes mellitus // Clinical. lab. diagn. 2002; 5: 25-32.

132. Emanuel V.L., Karyagina I.Yu., Emanuel Yu.V. Portable self-monitoring systems and laboratory analysis of blood glucose concentration *. Comparative research // Labor. honey. 2003; 6: 20-30.

133. Yavelov I.S., Zuikov Yu.A., Deev A.D., Travina E.E., Gratsiansky N.A., Averkov O.V., Vaulin N.A. Experience of studying heart rate variability in acute coronary syndromes // Ross, cardiol.magazine 1999; 1: 3-10.

134. Yabluchansky N.I., Martynenko A.V., Isaeva A.S. Fundamentals of the practical application of non-invasive technology for the study of human regulatory systems. – Kharkov: Osnova, 2000; 88.

135. Akselrod S., Gordon D., Ubel F.A. et al. Power spectrum analysis of heart rate fluctuation: a quantitative probe of beat to beat cardiovascular control // Science, 1981; 213: 220-222.

136. Allemann Y., Weidmann P. Cardiovascular, metabolic and hormonal dysregulations in normotensive offspring of essential hypertensive parents //

137.J Hypertens 1995; 13: 163-173.153 *. American Diabetes Association. Ray N., Thamer M., Gardner E., Chan J. Economic consequences of diabetes mellitus in the US in 1997: report from the American Diabetes Association // Diabetes Care 1998; 21: 296-309.

138. Amery A., Birkenhager W., Brixho P. et al. Glucose intolerance during diuretic therapy in elderly hypertensive patients. A second report the European Working

139. Party on High Blood Pressure in the Elderly. (EWPHE) // Postgrad Med J 1986; 62: 919-924.

140. Amos A. M., Carty D., Zimmet P. The rising global burden of diabetes and its complications: estimates and projections to the year 2010 // Diabetic Med 1997; 14: 1-85.

141. Anderson E.A, Hoffman R.P., Balon T.W., Sinkey C.A., Mark A.L. Hyperinsulinemia produces both sympathetic neural activation and vasodilatation in normal humans // J Clin Invest 1991; 87: 2246-2252.

142. Andronico G., Mangano M. T., Nardi E. et al. Insulin-like growth factor-1 and sodium-lithium counter transport in essential hypertension and in hypertensive left ventricular hypertrophy // J Hypertens 1993; 11: 1097-1101.

143. Anonymous. Clinical reality of coronary prevention guidelines: a comparison of EURO ASPIRE I and II in nine countries // Lancet 2001; 357: 995-1001.

144. Assman G., Culler P., Jossa E. et al. Coronary heart disease: reducing the risk // Fatheroscler Thromb Vase BioM999; 19: 1812-1824.

145. Babloyantz A., Destexhe A. Is the normal heart a periodic oscillator? // Biol. Cybern. 1988; 58: 203-211.

146. Bagg W., Ferri C., Desideri G. et al. The influences of obesity and “glycemic control on endothelial activation in patients with type 2 diabetes // J ‘Clin Endocrinol Metab 2001; 86: 5491-5497.

147. Barnell A. Hypertension and insulin resistance // Hyper ten Ann 1992: 2-18.

148. Bartnik M., Malmberg K., Ryden L. Managing heart disease Diabetes and the heart: compromised myocardial function a common challenge // Eur Heart J Supplements 2003; 5 (Suppl B): 33-41.

149. Beckman J. A., Creager M. A., Libby P. Diabetes and atherosclerosis. Epidemiology, pathophysiology and management // JAMA 2002; 287: 2570-2581.

150. Belfiore F., Mogensen C.E.New Concepts in Diabetes and Its Treatment. Basel, New York: S. Karger A. G., 2000; 264.

151. Berger M. Is hyperinsulinema a risk factor for atherosclerosis? // Ad van Diabetes 1992; 2: 43-48.

152. Bergman R.N., Finegood D.T., Ader M. Assessment of insulin sensitivity in vivo // EndocrRev 1985; 6: 45-86.

153. Bernardi L., Ricordi L., Lazzari P. et al. Impaired circulation modulation of sympathovagal modulation of sympathovagal activity in diabetes // Circulation 1992; 86: 1443-52.

154. Berthezene F. Hypertriglyceridemia: Cause or Consequence of Insulin Resistance? // Hormone Researcher 1992; 38: 39-40.

155. Brands M.W., Hall J.E. Hyperinsulinemia and hypertonia // NMCD 1993; 3: 155157.

156. Byyny R. L., Lo Verde M., Lloid S. et al. Citosolic calcium and insulin resistance in elderly patients with essential hypertension // Am J Hypertens 1992; 5: 459464

157 Bugram R., Akhlagi-Farsi H., Maresh H., Pfurscheller G. Eine Method zum Bestimmung des Pulswellelaufezeit // Aut-Biomed Tech 1994; 39: 51-56.

158. Capaldo B., Lembo G., Napoli R. et al. Skeletal muscle is a primary site of insulin resistance in essential hypertension // Metabol 1991; 40: 1320-1322.

159. Caro F. Jose. Insulin resistance in Obese and Nonobese Man // J Clin Endocrinol Metabolism 1991; 73: 691-695.

160. Castelli W.P. Lipid, risk factors and ischemic heart disease // Atherosclerosis 1996; 124: 1-9.

161. Chamontin B. Prevalence, treatment and control of hypertension in France population // J Hypertens 1998; 11: 759-762.

162. Cheatam B., Kahn C.R. Insulin action and the insulin signaling network // Endocr Rev 1995; 16: 117-142.

163. Chen C.-H., Tsai S.-T., Chuang J.-H. et al. Population-based study of insulin, c-peptide, and blood pressure in Chinese with normal, glucose tolerance // Am J Cardio 1995; 76: 585-588.

164. Chiasson J. L., Josse R., Gomis R. et al. Acarbose for prevention of type 2 diabetes mellitus for prevention of type 2 diabetes mellitus: the Stop – NDDM randomized trial // Lancet 2002; 359: 2072-2077.

165. Colhoum H.M., Dong W., Poulter N.R. Blood pressure screening, management and control in England: results from two health survey for England 1994 // J Hypertens 1998; 16: 747-752.

166. Couet C., Delarue J., Constans T. Age-related Insulin Resistance: A Review // Hormone Researcher 1992; 38: 46-50

167. De Fronzo R.A. Insulin resistance, hyperinsulinema, and coronary artery disease: A complex metabolic web // Cardiovasc Pharmacol 1992; 20: 1-16.

168.De Fronzo R.A., Ferrannini E. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia and atherosclerotic cardiovascular disease // Diabetes Care 1991; 14: 173-194.

169. De Henauw S., De Bacquer D., Fonteyve W., et al. Trends in the prevalence, detection, treatment and control of arterial hypertension in the Belgian adult population // J Hypertens 1998; 16: 277-284.

170. DECODE Study Group. Diagnosis and Classification of Diabetes Mellitus.American Diabetes Association diagnostic criteria // Diabetes Care 2007; 30: 42-47.

171. Diabetes Epidemiology Research International (DERI) Group // Diabet Metab Rev. 1990; 39: 858-864.

172. Dodson P.M. Hypertension and insulin resistance: mechanisms and implications for treatment // J Hum Hypertens 1991; 5: 1-6.

173. Donahue R.P., Orchard J. Hyperinsulinemia and insulin resistense associations with cardiovascular risk factors and disease // Cardiovasc. Risk Factors 1993; 1: 12-18.

174. Donnelly R. Angiotensine-Converting enzyme inhibitors and insulin sensitivity: metabolic effects in hypertension, diabetes, and heart failure // J Cardiovasc Pharmacol 1992; 20: 38-44.

175. Duplain H., Burcelin R., Sartori C. et al. Insulin resistance, hyperlipidemia, and hypertension in mice lacking endothelial nitric oxide syntheses // Circulation 2001; 342-345.

176. European Society of hypertension 2003 European Society of cardiology Guidelines for the management of arterial hypertension // J Hypertension 2003; 21: 1011-1053

177.Ferrannini E., Buzzigoli G., Bonadonna R., Giorico M.A. Insulin resistance in essential hypertension // Engine J Med 1987; 317: 370-377.

178. Ferrannini E., De Fronzo R.A. The association of hypertension, diabetes and obesity: A review // J Nephrology 1989; 1: 3-15.

179. Ferrannini E., Haffner S.M., Mitchell B.D., Stern M.P. Hyperinsulinemia: the key feature of a cardiovascular and metabolic syndrome // Diabetologia 1991; 34: 416-422.

180. Ferrannini E., Haffner S.M., Stern M.P. Insulin sensitivity and hypertension // Hypertension 1990; 8: 169-173.

181. Ferrannini E., Natali A. Essential hypertension, metabolic disorders, and insulin resistance // J Heart 1991; 121: 1274-1282.

182. Ferrara R., Guardigli G., Ferrari R. Understanding patient needs Myocardial metabolism: the diabetic heart // Eur Heart J Supplements 2003; 5 (Suppl B): 1518.

183. Ferrari AU. Modulation of parasympathetic and baroreceptor control of heart rate.// Cardioscience, 1993, 4 (1), 9-13.

184. Fisher M. Understanding patient needs prevention of macrovascular complications // Eur Heart J Supplements 2003; 5 (Suppl B): 29-31.

185. Fouad FM, Tarazi RC, Ferrario CM, Fighaly S, Alicandri C. Assessment of parasympathetic control of heart rate by a non-invasive method. // Am J Physiol. 1984; 246: 838-842.

186. Fuller J.H. Diabetes and Hypertension. Berlin, 1988: 8-11.

187. Gans R.O.B., Bilo H. J. G., Nauta J.J.P. et al. Acute hyperinsulinema induces sodium retention and a blood pressure decline in diabetes mellitus. // Hypertension 1992; 20: 199-209.

188. Gerstein H.C. A disturbed glucose metabolic state (dysglycaemia) is a key risk factor for cardiovascular events // Eur Heart J (Suppl B) 2003; 5: 1-2.135 ■. …

189. Gerstein H.C. Is glucose a continuous risk factor for cardiovascular mortality? // Diabetes Care 1999; 22: 659-660.

190. Giaconi S. Seasonal influences on blood pressure in high normal, to mild hypertensive range // Hypertension 1989; 14: 22-27.

191. Guzzetti S., Dassi S :, Pecis M. et al. Altered pattern of circadian neural1 control of heart period in mild hypertension // J. Hypertens 1991; 9: 831-838;

192. Haffner S. Insulimand Blood Pressure in the-San Antonio Heart Study: A Review // Cardiovascular Risk: Factors 1993; 1 :, 18-27.

193. He Z., Rask-Madseni C., King G.L. Managing heart disease Mechanisms of cardiovascular complications in diabetes and potential new. pharmacological therapies // Eur Heart J (Suppl.B) 2003; 5: 51-57.

194. Heart Rate Variability Standards of Measurement, Physiological Interpretation, and Clinical Use, Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology // Circulation 1996; 93: 10431065

195. Hink U., Li H., Mollnau H., et al. Mechanisms underlying endothelial dysfunction in diabetes mellitus // Circ Res 2001; 88: 14-22.

196. Holzmann M., Olsson A., Johansson J., Jensen-Urstad M.Left ventricular diastolic function is related to glucose in a middle-aged population // J Intern Med 2002; 251: 415-420.

197. Hughson RL, Yamamoto Y, McCullough RE, SLitton-JR, Reeves JT. Sympathetic and parasympathetic indicators of heart rate control at altitude studied by spectral analysis. // J Appl Physiol 1994; 77: 2537-2542.

198. Izzo J.L. Larrabee P.S., Sander E., Lillis L.M. Hemodynamics of seasonal adaptation // Am J Hypertens 1990; 3: 405-407.

199.Joffres M. R., Ghadirian P., Fodor J. G., et al. Awareness, treatment and control of hypertension in Canada // J Hypertens 1997; 10: 1097-1102.

200. Juhan-Vague I, Thompson SG, Jespercen J. Involvement of the hem static system in the insulin resistance syndrome. A study of 1500 patients with angina pectoris // Arterioscl Thromb 1993; 13: 1865-1873.

201. Julius S., Gudrabrandsson T., Jamerson K., Andersson O. The interconnection between sympathetic, microcirculation, and * insulin resistance in hypertension // Blood Pressure 1992; 1: 9-19.

202. Kannel W.B. Hypertension and the risk of cardiovascular disease. Hypertension, Diagnosis and Management. / Eds. J.H. Laragh, R.M. Brenner. – New York 1990; 1: 101-119.

203. Kaplan N.M. The deadly quarted: upper body obesity, glucose intolerance, hyperinsulinema, and hypertension // Arch Into Med 1989; 149: 1514-1520.

204. Kenny C. Primary care prevention of cardiovascular disease in diabetes // Practical Diabetes Int 2001; 18: 212-216.

205.Khoury S., Khaled I., Sowers J. The Patient with Syndrome X. The ABCs of Antihypertensive Therapy. New York, 1994: 213-220.

206. King H., Aubert R. E, Herman W.H ;. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projection // Diabetes Care 1998; 21: 1414-1431.

207. Kitney R’.I., Byrne S., Edmonds M.E. et al. Heart rate variability in’the assessment of autonomic diabetic neuropathy // Automedica 1982; 4: 155-167.

208. Ko G., Chan J., Jeung V. et al. Combined use of a fasting plasma glucose concentration and HbAlc or fructosamine predicts the likelihood of having diabetes in high-risk subjects // Diabetes Care 1998; 21: 1221-1225.

209. Kohner E.M. Prevention and Treatment of Diabetic Late Complications. Berlin, 1989: 75-91.

210. Laakso M. Hyperglycemia and cardiovascular disease in type 2 diabetes // Diabetes 1999; 48: 937-942.

211. Laakso M., Kuusisto J. Understanding patient needs Diabetology for cardiologists // Eur Heart J Supplements 2003; 5 (Suppl B): 5-13.

212. Landsberg L. Pathophysiology of obesity-related hypertension: Role of insulin and the sympathetic nervous system // J Cardiovascular Pharmacology. 1994; 23: 1-8.

213. Leon A.S., Connett J., Jacobs D.R. et al. Leisure-time physical activity levels and risk of coronary heart disease and death. The Multiple Risk Factor Intervention Trial // JAMA 1987; 258: 95 100.

214. Lillioja S., Young A.A., Culter C.L. et al. Skeletal muscle capillary density and fiber type are possible determinants of in vivo insulin resistance in man // J Clin.Invest 1987; 80: 415-424.

215. Lind L., Lithell H. Decreased peripheral blood flow in the pathogenesis of the metabolic syndrome including hypertension, hyperlipidemia, and hyperinsulinemia // Am Heart J 1993; 125: 1494-1497. I

216. Lindholm L. H., Ibsen H., Dahlof B., et al. Cardiovascular morbidity and mortality in patients with diabetes in the Losartan Intervention. For Endpoint reduction in hypertension study (LIFE) // Lancet 2002; 359: 1004-1010:

217. Lithell H.Metabolic aspects of the treatment of hypertension // J Hypertens 1995; 13: 77-80.

218. Luffer N., Engl H. G., Fisher F., Bauer R. d. Noninvasive continuous blood pressure control by pulse wave velocity // Zeitschrift Fur Karrdiologie 1996; 85: 124-126.

219. Lui J., Trevisan M., Menotti A. Syndrome X: prevalence in large population study // NMCD 1997; 7: 70-76.

220. Malik M., Camm A.J. Components of heart rate variability. What they really mean and what we really measure // J.Cardiol. 1993; 72: 821-822.

221. Malliani A., Lombardi F., Pagani M. Power spectral analysis of heart rate variability: a tool to explore neural regulatory mechanisms. // Br. Heart J 1994; 71: 1-2.

222. Marfella R, Esposito K, Giunta R, et al. Circulating adhesion molecules in humans: role of hyperglycemia and hyperinsulinemia // Circulation 2000; 101: 2247-2251.

223. Marigliano A., Tedde R., Sechi L. A. et al. Insulinemia and blood pressure: relationship in patients with primary and secondary hypertension, and with or without glucose metabolism impairment // Am J Hypertension 1990; 3: 521-526.

224. Moller D.E., Flier J’S. Insulin resistance mechanisms, syndromes, and implications // NEngle JMed 1991; 352: 938-948

225. Moreno P. R., Murcia A. M., Palacios I. F., et al. Coronary composition and macrophage infiltration in atherectomy specimens from patients with diabetes mellitus // Circulation 2000; 102: 2180-2184.

226. MuIler J.E., Toiler G.H., Stone P.H. Circadian variation and triggers of onset of acute cardiovascular diseases. // Circulation 1989; 79: 733-743.

227. Murray C.J., Lopez A.D. Mortality by cause for eight regions of the world: Global Burden of Disease study // Lancet 1997; 349: 1269-1276.

228. Nielsen F. General characteristics of the insulin resistance syndrome: prevalence and heritability. European Group for the study of Insulin Resistance (EGIR) // Drugs 1999; 58 (1): 7-10.

229. Niskanen L.K., Uusitupa M.I., Pyorala K. The relationship of hyperinsulinemia to the development of hypertension in type 2 diabetic patients and in non-diabetic subjects // J Hum Hypertens 1991; 5: 155-159.

230. Norhammar A. Managing heart disease Acute coronary syndromes: meticulous care is life-saving // Eur Heart J (Suppl B) 2003; 5: 29-31.

231. Norhammar A., ​​Tenerz A., Luben R. et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study // Lancet 2002; 359: 2140-2144.

232. O’Brien E., Sheridan S., O’Malley K. Dippers and non-dippers // Lancet 1988; 2: 397-399.

233. Pagani M., Lombardi F., Guzzetti S. et al. Power spectral analysis of heart rate and clinical pressure variabiliti as marker of sympathovagal interaction in men // Circ. Res. 1996; 59: 178-193.

234. Palatini P. Pessina A.C. A new approach to define the upper limit of ambulatory blood pressure monitoring. // J Hypertens 1990; 8: 65-70.

235. Palativi P., Julius S. Heart rate and the cardiovascular risk // Am J. Hypertens. 1997; 15: 3-7.

236. Parati G, Castiglioni P., Di Rienzo M.et al. Sequential spectral analysis of 24hour blood pressure and pulse interval in humans // Hiperyension 1990; 16: 414421.

237. Parati G., Omboni S., Di Renzo M. Twenty-four hour blood pressure variability: clinical implications // Kidney Int 1992; 41: 24-28.

238. Passa P. Hyperinsulinemia, insulin resistance and essential hypertension // Hormone Researcher 1992; 38: 33 38.

239. Perloff D. Sokolow M. The prognostic value of ambulatory blood pressure monitoring in treated hypertensive patients // J Hypertens 1991; 9: 1; 33-44.140 ‘■;

240. Perry G., Shankar R., Fineberg N. et al. HbAlc measurement improves the detection of type 2 diabetes in high risk individuals with no diagnostic levels of fasting’plasma glucose.//Diabetes,Care2001; 24: 465-471.

241. Pershadsingh HI A ;, Kurtz-T.W. Pharmacologic, reversal- of hyperinsulinema is associated with a reduction in blood pressure: a novel approach to treatment of hypertension // Hypertension 1992; 20: 410:

242. Pollare T., Lithell H.,. Berne C. Insulin resistance is a characteristic feature of; primary.hypertension-independent ofobesity // Metabolisnx1990; 39: 167-174 ‘

243. Pômerànz M., Macauly R. FB., GaudillMiA. Assessment’of autonomicfunctionin humans; by-heart rate spectral analysis.//Am: J. Physiol 1985; 246: 151-153.

244. Porush J.M., Faubert P.F. Hypertension, diabetes mellitus and nephropathy. -Sience Preess, London, 2001: 9-12.

245. Ratner R. Type 2 diabetes mellitus; the grand.overview // Diabetic Med 1998; 15 (Suppl 4): 4-7.■ ‘

246. Reaven G.M; The role of insuliniresistânce in human disease // Diabetes 1988; 37: 1595-1607. V

247. Reaven G., Ilollenbeck C.,. Chen Y. Relationship between glucose tolerance, insulin secretion, and insulin action in non-obese individuals with varying degrees; of glucose tolerance // Diabetologia: 1989;: 32: 52-55. …

248. Resnick L.M. Cellular ions hypertension, insulin resistance, obesity, and diabetes: a unifying theme // J Am Soc Nephrology 1992; 3: 578-585.’■

249. Resnick L.M; Ionic basis of hypertension, insulin resistance, vascular disease, and related disorders. The mechanism of “syndrome x” // Amer. J Hypertension 1993; 6 (4): 1235-1245.

250. Rett K., Wickmayr M., Mehnert M. New aspects of insulin; resistance in hypertension // Eur Heart J 1994; 15: 78-81.

251. Richard P. Donahue, Trevor J. Orchard. Myperinsulinemia and Insulin Resistance: Associations with Cardiovascular Risk Factors and Disease // Cardiovascular Risk Factors 1993; 1: 12-18.

252. Saad M. F., Anderson R. L., Laws A. et al. A comparison between the minimal model and the glucose clamp in the assessment of insulin-sensitivity across the spectrum of glucose tolerance ‘// Diabetes; 1994;: 43: IT14-1121.

253. Saad M.F., Lillioja S., Nyomba B.L. et al. Racial differences in the relation between blood pressure and insulin resistance // N Engl J Med 1991; 324: 733739. ‘

254. Sayers B.M. Analysis of heart rate variability // Ergonomics 1973; 16 (1):.17-32.

255. Schriër R.W., Estacio R.O. Additional follow-up from the ABCD trial in patients with type 2 diabetes and hypertension // N Engl J Med 2000; 343: 19-69.

256. Shalnova S.A., Deev D.A., Oganov R.S., Zhukovsky G.S. Arterial hypertension impact onmortality in Russia // Eur Heart LI998; 19: 705-707.

257. Skarfors E.T., Lithell H.O., Selinus I. Risk for the development of hypertension: a 10-year longitudinal study in middle-aged men // J Hypertens 1991; 9: 217-273.

258. Solymoss C., Marsil M., Chaur M. et al. Fasting ‘Hyperinsulinism, insulin Resistance Syndrome, and Coronary Artery Disease in Men and Women // Am J Cardiol l995; 75: 1152-1156

259 Sowers J.R. At the cutting edge: insulin resistance and hypertension. // Moll Cell Endocrin. 1990; 74: 87-89.

260. Sowers J.R., Zemel M.B. Clinical implications of hypertension in the diabetic patient // Am J Hypertension 1990; 3: 415-424.

261. Staessen J., Fagard R., Zijnen P. et al. Ambulatory blood pressure monitoring in clinical trials // J Hypertens 1991; 9: 1; 13-19.

262. Stamler J., Stamler R., Neaton J.D. Blood pressure, systolic and diastolic and cardiovascular risks: US population data // Arch Intern Med 1993; 153: 598 615.

263. Stern M.P. Diabetes and cardiovascular disease. The “common soil” hypotensis // Diabetes 1995; 44: 369-374.

264. Stern N., Tuck M. Drugs therapy of hypertension in diabetic patients // J Hum Hypertension 1991; 5: 295-305.

265. Strrattion I. M., Adler A. L., Neil H. A. et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study // BMJ 2000; 321: 405-412.

266. Swislocki A.L., Hoffman B.B., Reaven G.M. Insulin resistance, glucose intolerance, and hyperinsulinemia in patients with hypertension // Am J Hyperteens 1989; 2: 419-423.

267. Tasementzis S.A., Gill J.S., Hitchcock E.R. et al. Diurnal variation of activity during the onset of stroke // Neurosugery 1985; 17: 901-904.

268. The Fifth report of the Joint National Committee on detection, evolution and treatment of high blood pressure // Arch Int Med 1993; 159: 154-183.

269. The Sixth Report of the Joint National Committee on Prevention, Detection, Evolution, and Treatment of High Blood Pressure // Arch Intern Med 1997; 157: 2413-2446.

270. Tochikubo O., Miyazaki N., Yamada Y., et al. Mathematical evaluation of 24hour blood pressure variability in young, middle-aged and elderly hypertensive patients // Jap.Circular J 1985; 51: 1123-1129.

271. Tominaga M., Eguchi H., Manaka H. et al. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study // Diabetes Care 1999; 22: 920-924.

272. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular complications in type 2 diabetes: UKPDS 38 // Br Med J 1998; 317: 703-713.

273. Van den Akker T.J., Koelman A.S.M., Hogenhuis L.A.H., Rompelman G. Heart rate variability and blood pressure oscillations in diabetics with autonomic neuropathy // Auto-medica 1983; 4: 201-208.

274. Watanabe N. Imai Y. Nagai K. et al. Nocturnal blood pressure and silent cerebrovascular lesions in elders Japanese. // Stroke 1996; 27: 1319-1327.

275. Weidemann P., Bohlen L., de Courten M. Insulin resistance and hyperinsulinemia in hypertension // J Hypertension 1995; 13: 65-72.

276. Widen E., Ekstrand A., Saloranta C.et al. Insulin resistance in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridemia // Diabetologia 1992; 35: 1140-1145.

277. Zanchetti A. The role of ambulatory blood pressure monitoring in clinical practice // Am J Hypertens 1997; 10: 1069-1080.

278. List of published works on the topic of the thesis

279. Elbaeva A.D. Dynamics of changes in blood glucose in arterial hypertension // Perspective-2003: Reports of the All-Russian scientific conference: T.8. Nalchik: Cab.-Balk. un-t, 2003. – S. 143-147.

280. Elbaev A.D., Kurdanov Kh.A., Elbaeva A.D. Blood pressure monitoring in patients with type 2 diabetes // Successes of modern natural science. – 2006. No. 12. – S. 79-80.

281. Kurdanov Kh.A, Elbaeva A.D., Batyrbekova L.M., Kurdanova M.Kh., Elbaev A.D. A new method of daily monitoring of blood pressure and glycemic levels // Fundamental Sciences to Medicine: Proceedings of the RAS conference. -M .: Slovo, 2006.- S. 100-102.

282. Elbaev A.D., Kurdanov Kh.A., Elbaeva A.D. Diagnostic aspects of the relationship between hemodynamic parameters and blood glucose levels // Clinical physiology of blood circulation. 2006. – No. 3. – S. 15-20.

283. Elbaeva A.D. Variability of blood pressure and blood glucose levels in diabetes mellitus // Perspective-2007: Reports of the International Congress of Students, Postgraduates and Young Scientists. T. 4. -Nalchik: Cab.-Balk. un-t, 2007.S. 151-152.

284.Elbaeva A.