Morphology of diabetes. Obesity as a cause of diabetes

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Morphology of diabetes. Obesity as a cause of diabetes

Of great importance in the etiology of diabetes are acute infections (tonsillitis, influenza, malaria, typhoid fever). Currently, it is believed that these infections affect the centers of the hypothalamus. Injuries to the hypothalamus can also cause diabetes when combined with other factors predisposing to its occurrence. Camus and Roussy, M. S. Kahana and others experimentally caused diabetes mellitus hypothalamic origin. Circulatory disturbance, persistent narrowing of the vessels of the islet apparatus can lead to a decrease in its functions. With hypertension, A. I. Gefter established a decreased release of insulin. N. A. Tolubeeva and A. L. Pavlovskaya, examining patients with hypertension, found that their fasting blood sugar was higher than normal or at the upper limit of normal, and the sugar curves in some patients were similar to diabetic. In diabetes mellitus, structural changes are often found in pancreatic tissue and in the islet apparatus. They are observed in 74% of patients. Atrophic, degenerative, inflammatory processes develop in the glandular islet tissue, connective tissue grows, and fatty infiltration occurs. The development of pancreatitis leads to these changes. S. M. Leites believes that some forms of diabetes mellitus are of alloxan origin. Alloxan can be formed in the body with pathology of purine metabolism. Usually, its excess amount is neutralized by amino acids containing sulfhydryl groups (cysteine, glutathione). If for some reason there is a lack of nutrients, then alloxan is not neutralized in this way, the latter can exert its effect on the b-cells of the islet apparatus and cause diabetes mellitus. Joslin attaches importance to obesity in the etiology of diabetes. He believes that every obese person is a candidate for diabetes. At the same time, he refers to Young’s experiments in which, under the influence of pituitary extracts, dogs first gained weight, and then diabetes developed. In experimental obesity in geese, we observed fatty degeneration of the liver and hyperglycemia (M. S. Kahana). According to statistics, 15-30% of patients with diabetes show heredity with recessive or dominant transmission. Naunyn, for example, believes that all the etiological factors of diabetes mellitus are only permissive for the underlying hereditary predisposition. Inactivation of insulin is often found. It can be an additional factor enhancing insulin deficiency of islet origin (contrainsular substances). This explains the occurrence of diabetes with a number of pituitary diseases (acromegaly, Itsenko-Cushing’s disease) and with adrenal cortical adenoma. Hyperglycemia and glucosuria are symptoms indicating a violation of carbohydrate metabolism in diabetes mellitus. Instead of the usual blood sugar content of 110-120 mg%, patients have an increase to 200-300 mg% of glucose in the blood and even more. If lipocaine insufficiency also joins, then in this case obesity of the liver occurs. In blood, the amount of fat instead of 1% normally reaches 15-18%. The increased intake of fatty acids and triglycerides in the liver leads to increased oxidation and increased formation of ketone bodies, ketonemia and ketonuria in the liver. Instead of normal 2-10 mg%, the content of ketone bodies reaches 15-20% or more. An increase in the concentration of ketone bodies in the blood causes ketonuria. Most researchers indicate that in patients with diabetes, hypercholesterolemia can be detected. According to A.M. Gelfand, of the 220 examined patients with diabetes, in 102 fasting blood cholesterol was higher than 220 mg%, and in 20 – above 300 mg%.

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