Diabetes got its name because of the presence of glucose in the urine with this disease. Two main types of diabetes are known that have a similar course of hyperglycemia and vascular complications. They differ in the pathogenesis and ability of residual insulin to inhibit the formation of ketone bodies from fatty acids.
Type I diabetes mellitus (insulin-dependent, with a tendency to ketoacidosis) occurs as a result of autoimmune destruction of pancreatic (3-cells. Autoimmune process begins several years before the cessation of insulin production, and by the time diabetes is diagnosed, most (3-cells are already irreversibly damaged. Since this usually occurs before the age of 30, this type of diabetes is called juvenile diabetes.The main feature of type I diabetes is the inability of the pancreas to produce even a small amount of insulin a, required to suppress the formation of ketones, which leads to relapse of diabetic ketoacidosis.
In type II diabetes mellitus, insulin is produced, but it is ineffective for normalizing blood glucose levels. However, the amount of insulin available in most cases is sufficient to suppress the formation of ketones, therefore, such patients do not have recurrent attacks of diabetic ketoacidosis. Insulin is sometimes prescribed for such patients, but usually they do not need it to prevent ketoacidosis. The function (3 cells in type II diabetes decreases over time to such an extent that some patients develop insulin deficiency, and ketoacidosis can develop with an infectious or other serious disease.
In the early stages of type II diabetes, the main feature of this disease is an inadequate change in blood glucose levels in response to insulin administration. This phenomenon is called “insulin resistance.” It occurs due to a mutation of the receptor, which weakens its response to insulin. Type II diabetes and insulin resistance cause the syndrome, which may include:
• defects in glucose transport;
• densitization of insulin receptors;
• toxic effects of hyperglycemia;
• metabolic disorders leading to increased body weight;
• conditions associated with an excess of counter-insular hormones (eg, pheochromocytoma, Cushing’s syndrome and acromegaly);
• conditions associated with the loss of pancreatic function (for example, surgical removal of cancers on the gland or the gland itself).
Signs of hyperglycemia are common to all types of diabetes. Hyperglycemia leads to insulin deficiency (type I) or insulin resistance (type II). Impaired glucose uptake by target tissues after eating leads to postprandial (occurring after eating) hyperglycemia, however, the main cause of diabetic hyperglycemia is insufficient insulin glyconeogenesis. Fasting plasma glucose concentrations of more than 7 mmol / L (125 mg / dl) are associated with an increased risk of long-term diabetic complications. Symptomatic hyperglycemia (polyuria, polydipsia, weight loss) usually occurs with high blood glucose levels. Glycosuria occurs only when the concentration of glucose in the renal tubules is above the threshold of maximum absorption, which occurs at approximately 9 mmol / l (160 mg / dl). For this reason, urinary glucose control may not always be a criterion for the effectiveness of antidiabetic therapy.
An increase in plasma glucose concentration increases the level of glycosation (non-enzymatic covalent glucose compounds) of many proteins in the body. Elevated levels of glycated hemoglobin (HbA1c) reflects the presence of prolonged hyperglycemia and is useful for glycemic control in diabetes.