The Pathophysiology of Diabetes

Diabetes Mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in the secretion of insulin, the action of insulin, or both. There are four major of diabetes. Type 1 diabetes, which makes up 5% to 10% of diagnosed cases, was formerly called juvenile-onset diabetes or insulin dependent diabetes. Type 2 diabetes, which is 90% to 95% of diagnosed cases, was formerly labeled non-insulin-dependent diabetes or adult onset diabetes. The other two major types are gestational diabetes, which affects 2% to 5% of all pregnancies, and other specific types of diabetes which make up 1% to 2% of all diagnosed cases.

Type 1 Diabetes:

Type 1 diabetes most often occurs in childhood and adolescence, but it may occur at any age, even in the 80s and 90s. This disorder is characterized by hyperglycemia, which is elevated blood glucose (sugar) levels, and breakdown of body fats and proteins, and the development of ketosis, an accumulation of ketone bodies produced during oxidation of fatty acids.

Type 1 diabetes is the result of the destruction of the beta cells of the islets of Langerhans in the pancreas. When beta cells are destroyed, insulin is no longer produced. Although type 1 diabetes may be classified as either an autoimmune or idiopathic disorder, 90% of the cases are immune mediated. The disorder begins with insulinitis, a chronic inflammatory process that occurs in response to the autoimmune destruction of islet cells. This process slowly destroys beta cell production of insulin, with the onset of hyperglycemia occurring when 80% to 90% of beta cell function is lost. This process usually occurs over a long preclinical period. It is believed that both alpha-cell and beta-cell functions are abnormal, with a lack of insulin and a relative excess of glucagon resulting in hyperglycemia.

Type 2 Diabetes:

Type 2 diabetes is a condition of fasting hyperglycemia that occurs despite the availability of endogenous insulin. Type 2 diabetes can occur at any age, but it is usually seen in middle-age and older people. Heredity plays a role in its transmission.

Although the exact cause of type 2 diabetes is unknown, several theories have been suggested. These theories include limited beta-cell response to hyperglycemia, peripheral insulin resistance, and insulin receptor or postreceptor abnormalities. Whatever the cause there is sufficient insulin production to prevent the breakdown of fats with resultant ketosis; type 2 diabetes is characterized as a non-ketotic form of diabetes. However, the amount of insulin available is not sufficient to lower blood glucose levels through the uptake of glucose by muscle and fat cells.

A major factor in the Pathophysiology of type 2 diabetes is cellular resistance to the effect of insulin. This resistance is increased by obesity, inactivity, illnesses, medications, and increasing age. In obesity, insulin has a decreased ability to influence glucose metabolism and uptake by the liver, skeletal muscles, and adipose tissue. Although the exact reason for this is not clear, it is known that weight loss may improve the mechanism responsible for insulin receptor-binding or postreceptor activity.