Insulin is a hormone (from the Greek word for “trigger, induce”), which is a product of the pancreas (endocrine gland) and is released by it directly into the blood. Insulin is a protein produced by the beta cells of the so-called islets of the endocrine pancreas (from the Latin word “insula” — island). The intensity of insulin formation is influenced by the level of glucose in the blood and other hormones — glucagon (formed in the alpha cells of the islets of the pancreas), hormones of the thyroid gland, adrenal glands, etc.
Insulin provides the transport and oxidation of glucose in cells, the formation of a storage carbohydrate glycogen in the liver. It inhibits the formation of glucose from amino acids of protein and fatty acids of fats, enhances the synthesis of body proteins from amino acids, affects the formation of adipose tissue from glucose and fatty acids. Thus, insulin regulates not only carbohydrate, but also protein and fat metabolism.
The action of insulin on sensitive tissues (liver, muscle and adipose tissue) is carried out through the insulin receptors perceiving it (from the Latin word “reception” — acceptance, reception) of cells. Glucose enters the brain, nerve and blood cells, kidneys, blood vessels regardless of the effect of insulin. But with a deficiency of insulin in the body, a decrease in the activity and / or the number of its receptors, an unrestrained excess of glucose in the blood enters the “insulin-independent tissues”, which leads to the development of chronic complications of diabetes mellitus.
- Blood glucose is referred to as “glycemia” (from the Greek words “glycos” — sweet and “emia” — blood). In colloquial speech, “blood glucose” is usually replaced by the phrase “blood sugar”, which is incorrect from a medical point of view.
- Increased, higher than normal blood glucose is referred to as “hyperglycemia” (from the Greek word “hyper” —above).
Glucose is the main source of energy for all organs and tissues, but most of them, as indicated above, glucose is received only with the help of insulin. Insulin, as a key, opens the “door” for glucose to enter cells, where, during its oxidation, the energy necessary for the body is formed.
- If there is little insulin, or it has defects, or the activity and / or the number of receptors perceiving insulin are genetically reduced in the cells, then part of the glucose does not penetrate into the cells (“remains behind a closed or half-open door”) and its level in the blood rises. Hyperglycemia occurs. The cells begin to starve when there is an excess of “food” in the blood — glucose.
- In response to starvation, the formation of glucose in the liver and muscles from a storage carbohydrate — glycogen, can begin, and after a decrease or depletion of glycogen stores from fats (fatty acids) and proteins (amino acids). The level of glucose in the blood increases even more (that is, hyperglycemia increases), and part of it is excreted in the urine, which is denoted by the term glucosuria (from the Greek words “glucos” — sweet and “urine” — urine). If this process is not stopped with the help of insulin introduced into the body, then deep disturbances of fatty and other types of metabolism develop — ketoacidosis.
However, the main source of glucose entering the blood remains food containing various carbohydrates (starch, sucrose, lactose, etc.), which, after being digested in the gastrointestinal tract, are mostly converted into glucose. Some of it is absorbed from the digestive tract directly into the bloodstream when using “pure” glucose, for example from honey, fruits or berries. Therefore, the nature of the diet (the amount and types of carbohydrates, diet, etc.) largely determines the blood glucose (glycemia) content, preventing or reducing hyperglycemia, as well as preventing a decrease in blood glucose levels — hypoglycemia (the Greek word “hypo ”- below).
Determining the level of glycemia is the basis for the diagnosis of diabetes. In 1999, experts from the World Health Organization proposed new approaches to diagnosing diabetes mellitus and determining other categories of hyperglycemia. Currently, these approaches, presented in table 2, entered the practice of doctors in Russia and other countries of the world.
The diagnosis of diabetes mellitus can be made when the fasting glucose level in whole blood is 6.1 mmol / L (110 mg / dL) or more, or in blood plasma of 7.0 mmol / L (126 mg / dL) or more.
In everyday practice, to establish a diagnosis of diabetes mellitus, it is sufficient to use data on the concentration of glucose in the blood on an empty stomach, and not the results of a glucose tolerance test. This test must be used during pregnancy, when fasting glycemia does not differ from normal values.
The diagnosis of diabetes mellitus must be confirmed by re-determination of glycemia (blood glucose) on other days. Determination of the level of glycemia for the diagnosis of diabetes mellitus is not carried out:
- due to an acute illness, injury or surgery;
- after short-term intake of drugs (glucocorticosteroids — prednisolone, etc., thyroid hormones — eutirox, etc., diuretics, namely thiazide diuretics — hypothiazide, etc.);
- in patients with liver cirrhosis.
Let us pay special attention to the fact that in recent years, an increased level of fasting blood glucose, which does not reach the degree of diabetes mellitus, and even more impaired glucose tolerance after a food load of glucose has been called prediabetes. It was found that every year about 2 — 7% of people with impaired glucose tolerance develop type 2 diabetes mellitus, and the level of fasting glycemia 5.6 mmol / l or more increases the risk of transition of impaired glucose tolerance to sugar by 3.3 times. type 2 diabetes.
The American Standards of Care for Diabetes Mellitus (2007) states: “Recently elevated fasting glucose and impaired glucose tolerance are officially termed prediabetes. Both of these conditions are risk factors for the development of diabetes mellitus and cardiovascular disease”. Therefore, from a modern point of view, therapeutic and prophylactic measures should be extended to prediabetes, in particular, as one of the frequent manifestations of metabolic syndrome. Note that a similar situation has arisen at the present time with such concepts as “prehypertension” as a pre-disease and arterial hypertension as an already existing disease.
Recently elevated fasting glucose and impaired glucose tolerance are officially termed prediabetes. Both of these conditions are risk factors for the development of diabetes mellitus and cardiovascular disease
The American Standards of Care for Diabetes Mellitus
Diabetes mellitus compensation is the maintenance of glycemia with the help of drugs and diet, as well as dosed physical activity at levels that are as close as possible to the values typical for healthy people. In other words, it is the normalization of carbohydrate metabolism in diabetic patients.
The level of glycated hemoglobin (HbA1c) in the blood is considered an informative indicator of the effectiveness of blood glucose control, i.e. the correctness of diabetes mellitus treatment. Note that glycated hemoglobin is also referred to as “glycosylated hemoglobin”.
Hemoglobin is found in red blood cells. Throughout the life of erythrocytes (110-120 days), glucose freely penetrates into them and binds to hemoglobin. In this case, glycated hemoglobin is formed, which in healthy people is less than 6% of the total hemoglobin content. In case of hyperglycemia, typical for diabetes mellitus, the percentage (HbA1c) in relation to the total amount of hemoglobin increases (see Table 3)
Glucose in the urine is not excreted if its level in the blood does not exceed a certain value. With hyperglycemia above a certain threshold (“renal threshold”), the kidneys begin to excrete glucose in the urine — glucosuria occurs. The magnitude of the renal threshold varies from person to person. It is generally accepted that in healthy young and middle-aged people, the renal glycemic threshold is, on average, 10 mmol / l. In the elderly, the renal glycemic threshold is 13.9 mmol / L or more, while in pregnant women it is reduced to 5.6 — 6.7 mmol / L.
Thus, by the presence of glucose in the urine, one can to some extent judge the degree of hyperglycemia. However, the determination of the level of glucosuria to control the compensation of diabetes mellitus has only an approximate value, this indicator is especially unreliable if the patient has kidney disease. For the selection of doses of insulin, you cannot use indicators of glucosuria.