Diabetes mellitus (DM) is characterized by impaired insulin secretion and a varying degree of insulin resistance. In type 1 diabetes mellitus, autoimmune destruction of pancreatic beta cells leads to loss of insulin secretion. In type 2 diabetes mellitus, insulin secretion is insufficient, as patients have developed resistance to insulin.
Insulin stimulates glucose utilization and suppresses its synthesis. In addition, it regulates the transport of glucose from the blood to most tissues except the liver, central nervous system, and red blood cells. As a result, impaired insulin synthesis impairs glucose utilization significantly increasing its blood concentration. Muscle and adipose tissue, the two most important glucose users, disrupt glucose uptake, and utilization. The liver also loses its ability to use blood glucose. At the same time, gluconeogenesis and proteolysis in the muscles increase rising blood glucose levels. The reabsorption of glucose in the kidneys leads to its excretion in the urine (glucosuria).
Insulin also affects lipid metabolism in adipose tissue. It stimulates the synthesis of fatty acids from glucose and enhances the generation of NADPH+. Another function of insulin is the inhibition of fat breakdown and muscle protein degradation. Thus, insulin deficiency leads to deep disturbances in lipid metabolism, which is observed in patients with diabetes mellitus. Decreased glucose utilization leads to the production of ketone bodies that affect the physiological pH.