Causes of Type II Diabetes Mellitus
Diabetes mellitus type II is, by its mechanism of development, a group of metabolic disorders that can occur under the influence of a wide variety of causes. This disease is characterized by a wide variety of manifestations.
Type II diabetes mellitus is divided into two groups: diabetes mellitus IIa and diabetes mellitus IIb. Diabetes mellitus IIa occurs without obesity. Often under his mask, diabetes mellitus latent autoimmune( as a result of impaired function of the body's immune system) character. Diabetes mellitus IIb is characterized by the presence of obesity. Streets suffering from diabetes mellitus IIa, the achievement of a normal level of glucose in the blood presents certain difficulties, which is observed even with the use of tableted sugar-reducing drugs at the maximum dose. After about 1-3 years after the beginning of treatment with tableted sugar-reducing drugs, the effect of their use disappears completely. In this case, resort to the appointment of insulin preparations. In type II diabetes mellitus, in more frequent cases, diabetic polyneuropathy( a widespread lesion of the nervous system) develops more rapidly than diabetes IIb type. Diabetes mellitus type II is characterized by a hereditary predisposition. The probability of developing this type of diabetes in a child in the presence of the same disease in one of the parents is about 40%.The presence of obesity in humans contributes to the development of a violation of tolerance( resistance) to glucose and type II diabetes mellitus. Obesity of the first degree increases the risk of developing type II diabetes three times. If there is obesity of an average degree, then the probability of diabetes mellitus increases fivefold. With obesity of the third degree, the likelihood of developing type II diabetes is more than 10 times higher.
The mechanism of development of type II diabetes includes several stages.
The first stage is characterized by a person's innate tendency to obesity and high blood glucose.
The second stage involves low mobility, an increase in the amount of food consumed in combination with a violation of the production of insulin β -cells of the pancreas, which leads to the development of resistance of the body tissues to the action of insulin on them.
In the third stage of development of type II diabetes, there is a violation of resistance to glucose, which leads to a metabolic syndrome( metabolic syndrome).
The fourth stage is characterized by the presence of diabetes mellitus type II in combination with hyperinsulinism( an increase in the insulin content in the human blood).
In the fifth stage of the development of the disease, the function of the B cells is depleted, which leads to the need for an insulin introduced from the outside.
The leading in the development of type II diabetes is the availability of resistance of the body tissues to insulin. It is formed as a result of a decrease in the functional capacity of the β pancreatic cell.
There are several mechanisms of disturbance of the function of cells producing insulin.
1. In the absence of pathology, insulin is produced by β -cells of the pancreas with a certain periodicity, which is usually 10-20 minutes. In this case, the content of insulin in the blood undergoes fluctuations. In the presence of breaks in the production of insulin, the sensitivity to this receptor hormone is restored, which are located on the cells of various tissues of the human body. Type II diabetes mellitus may occur with an increase in the insulin content in the blood stream, while there is no periodicity in its production. At the same time, there are no fluctuations in its content in the blood, which are characteristic of a normal organism.
2. If the blood glucose level increases after a meal, there may not be an increase in the release of insulin by the pancreas. In this case, already formed insulin is not able to be ejected from β -cells. His formation continues in response to an increase in blood glucose, despite its excess. The glucose content for this pathology does not reach normal values.
3. Premature emptying of β -cells of the gland may occur when active insulin has not yet formed. Isolated at the same time in the bloodstream, proinsulin does not have activity against glucose. Proinsulin may have atherogenic effects, i.e., contribute to the development of atherosclerosis.
With an increase in the amount of insulin in the blood( hyperinsulinemia), excess glucose is continuously supplied to the cell.
This leads to a decrease in the sensitivity of insulin receptors, and then to their blockade. In this case, the number of insulin receptors located on the cells of the organs and tissues of the body gradually decreases. Against the background of hyperinsulinemia, glucose and fats that enter the body as a result of food intake are excessively deposited in adipose tissue. This leads to an increase in the body's resistance to insulin. In addition, hyperinsulinemia suppresses the breakdown of fats, which in turn contributes to the progression of obesity. An increase in blood glucose levels adversely affects the functional capacity of the β -cell gland, leading to a decrease in their activity. Since the high blood glucose level is constantly observed, for a long time insulin is produced by cells in the maximum amount, which eventually leads to their depletion and stopping the production of insulin. For treatment use insulin preparations. Normally, 75% of the glucose consumed is disposed of in the muscle, deposited in the liver as a reserve substance - glycogen. As a result of the stability of muscle tissue to the action of insulin, the process of formation of glycogen from glucose in it decreases. Stability of the tissue to the hormone arises as a result of mutation of genes in which special proteins encoding glucose transport into the cell are encoded. In addition, as the level of free fatty acids increases, the formation of these proteins decreases, which leads to a violation of the sensitivity of pancreatic cells to glucose. This leads to a violation of the secretion of insulin by a given gland.