Physiology and Pathophysiology of Diabetes Mellitus

Physiology and Pathophysiology of Diabetes
Insulin is secreted by the beta cells, which is one of four types of cell in Islet of Langerhans in the pancreas. Insulin is a storage hormone. When a person eats a meal, secretion of insulin increases and moves glucose from the blood into muscle, liver and fat cells. In those cells, insulin:
• Transports and metabolizes glucose for energy

• Stimulates storage of glucose in the liver and muscle (in the form of glycogen)
• Signals the liver to stop the release of glucose
• Enhances storage of dietary fat in adipose tissue
• Accelerates the transport of amino acids (derived from dietary protein) into cells.
Insulin also inhibits the breakdown of stored glucose, proteins and fat. When the person do not eat or during fasting periods, the pancreas continuously secrete small amounts of insulin (basal insulin); another pancreatic hormone secreted by the alpha cells of the Islets of Langerhans called glucagon is released when the blood drops and stimulate the liver to release stored glucose. Insulin and glucagon maintain a constant level of glucose in the blood. The liver produces glucose through the “breakdown of glycogen” (glycogenolysis). Liver utilizes the breakdown of carbohydrate substance including amino acids in the process called (glucogenesis).

Gestational Diabetes

Gestational Diabetes

Gestational Diabetes is diabetes that the onset of glucose intolerance is during pregnancy. During pregnancy there is secretion of placental secretion which causes insulin resistance (do not bind with the special receptors of the cell). Women that are pregnant between 24^th and 28^th week: age 25 years and has a family history of diabetes in first degree relatives, should undergone selective screening to rule out gestational diabetes.

Type 2 Diabetes

Type 2 Diabetes Mellitus
Also known as:
• Adult onset Diabetes Mellitus
• Non-Insulin Dependent Diabetes Mellitus
• Ketosis Resistant Diabetes Mellitus

Type 2 Diabetes Mellitus is a adult onset, and non-insulin dependent. There are 2 main problems related to insulin in type 2 diabetes, first one is “insulin resistance “ (insulin do not bind with the special receptor on cell surface) and impaired insulin secretion (insulin secreting glands release irregular amount of insulin). Exact mechanism that leads to this problem s is unknown, but there are some factors that can predispose to type 2 Diabetes Mellitus in the family. However, despite of the impaired insulin secretion, there is enough insulin present in the blood to prevent the “lipolysis” (breakdown of fat) and the accompanying production of “ketone bodies” (by product of fatty acids). Therefore, Diabetic Ketoacidos does not typically occur in type 2 Diabetes Mellitus. Uncontrolled type 2 Diabetes Mellitus may lead to other acute problems including Hyperglycemic, Hyperosmolar Non-ketotic syndrome (HHNS).

Type 1 Diabetes

Type 1 Diabetes Mellitus accounts for 5-10 % of all diabetic cases.

Also known as:

• Juvenile Diabetes Mellitus
•  Ketosis Prone Diabetes
•  Insulin Dependent Diabetes Mellitus (IDDM)

Type 1 diabetes is characterized by destruction of the pancreatic beta cells. Most likely cause of these conditions is combined genetic, immunologic and possibly environmental (e.g. viral) factors contribute to cell destruction. People do not inherit type 1 Diabetes itself; rather they inherit a genetic predisposition or tendency toward developing type 1 Diabetes. There is some evidence of autoimmune response on type1 Diabetes. This is abnormal response of the body in which the antibodies are direct against the normal tissues as if they were foreign and eventually can damage Islet of Langerhans , specific area of the pancreas that produce insulin, reducing the production of insulin or totally no production of insulin. Insulin deficiency may occur as a result of inhibition of glycogenolysis (breakdown of stored glucose) and glucogenesis (production of new glucose from amino acids and other substrates). These process occur in erratic fashion and further contribute to hyperglycemia. In addition, fat breakdown occurs, resulting in an increased production of “ketone bodies”  (byproducts of free fatty acids), the process called lypolysis.

What is Diabetic Mellitus?

Diabetes Mellitus is a metabolic disease characterized by increase levels of glucose in the blood, termed as (hyperglycemia) which means “hyper” (elevated) “glyco” or “glucose” (sugar) and “emia” (blood) elevated sugar in the blood. It results from defects in insulin secretion, insulin action or both. Normally a certain amount of sugar circulates in the blood, around 70-120 mg/dl. The major sources of this glucose are absorption of ingested food in the gastrointestinal tract and formation glucose by the liver from the food substances termed as (gluconeogenesis) “gluco” (sugar) “neo” (new) and “genesis” (formation).

Insulin a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and storage of glucose. In the diabetic condition the cells may stop responding to insulin or the pancreas may stop producing insulin entirely. This leads to hyperglycemia , which may result in acute metabolic complications such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Long term effects ofhyperglycemia contribute to macrovascular complications (coronary artery disease, cerebrovascular disease, and peripheral vascular diseases), chronic microvascular complications (kidney and eye disease) , and neuropathic complications (diseases of the nerves).