Complications of diabetes mellitus: A review

Abstract

Diabetes mellitus (DM) is a chronic disease characterized by hyperglycemia and complications that include microvascula disease of the eye and kidney and a variety of clinical neuropathies. DM, also known as simply diabetes, is a group o metabolic diseases in which there are high blood sugar levels over a prolonged period. These high blood sugar level produce the symptoms of repeated urination, increased hunger, and increased thirst. Untreated diabetes can cause many complications. Acute complications include diabetic ketoacidosis (DKA) and non-ketotic hyperosmolar coma. Serious long term complications include heart disease, stroke, kidney failure, foot ulcers, and damage to the eyes. Metabolic abnormalitie in carbohydrates, lipids, and proteins result from the important role of insulin as an anabolic hormone. Low levels of insulin to achieve adequate response and/or insulin resistance of target tissues, mainly skeletal muscles, adipose tissue, and to a lesse extent, liver, at the level of insulin receptors, signal transduction system, and/or effector enzymes or genes are responsible for these metabolic abnormalities. The severity of symptoms is due to the type and duration of diabetes. Some of the diabete patients are asymptomatic, especially those with type 2 diabetes during the early years of the disease. Others with marked hyperglycemia, especially in children with absolute insulin deficiency, may suffer from polyuria, polydipsia, polyphagia weight loss, and blurred vision. Uncontrolled diabetes may lead to stupor, coma, and if not treated death, due to ketoacidosi or rarely from non-ketotic hyperosmolar syndrome. Several pathogenic processes are involved in the development o diabetes. These range from autoimmune destruction of the beta-cells of the pancreas with consequent insulin deficiency to the abnormalities that end in resistance to insulin action. The basis of the abnormalities in carbohydrate, fat, and protein metabolism in diabetes is deficient action of insulin on target tissues. Deficient insulin action results from inadequate insulin secretion and/or diminished tissue responses to insulin at one or more points in the complex pathways of the hormone action Impairment of insulin secretion and defects in insulin action frequently coexist in the same patient, and it is often unclea which abnormality is the primary cause of hyperglycemia.