Pancreas is the organ which is responsible for development of diabetes. When there is dysfunction of pancreas, particularly beta-cells of pancreas which produce and secrete insulin, which is responsible for metabolism of glucose.

The diseases of pancreas include pancreatitis (infection/inflammation of pancreas which may be acute or chronic), diabetes mellitus, cystic fibrosis, cancer of pancreas etc.

Anatomy of Pancreas:

Pancreas is approximately six inches long, flat and narrow organ with a head, tail and middle section. The location of pancreas is between stomach and spine. Small ducts feed pancreatic juice to the pancreatic duct inside the pancreas, which connects to duodenum, through head section. The common bile duct also runs through the head section of the pancreas and carries bile from the liver and gall bladder into the small intestine.

Pancreas has 2 types of tissues: exocrine and endocrine.

Exocrine tissue: this tissue produces powerful pancreatic enzymes for digestion of fats, proteins, and carbohydrates. The enzymes produced by the exocrine tissue include lipases; proteinases etc. and they also produce bicarbonates for neutralization of gastric acids.

Endocrine tissue: the endocrine tissue of pancreas consist of specialized clusters of islet cells that produce a variety of hormones, with each cluster specializing in the production of a specific hormone, such as insulin produced by beta-cells of pancreas, alpha cells (glucagon-producing), delta cells (somatostatin-producing), and PP cells (pancreatic polypeptide-producing).

Functions of pancreas:

• The enzymes secreted by pancreas are used for digestion of fats, carbohydrates and proteins. Pancreas also secretes bicarbonate which neutralizes the gastric acid in duodenum.
• Pancreas secretes insulin and glucagon. Insulin and glucagon regulate the glucose metabolism.

The endocrine tissue and the endocrine functions of pancreas are involved in the causation and pathogenesis of diabetes mellitus.

Type-1 Diabetes Pathogenesis:

Type I Diabetes occurs when insulin production either shuts down or is severely reduced due to destruction of insulin producing beta-cells, the islets of Langerhans. The destruction of islets of Langerhans generally occurs (starts) due to genetic susceptibility and followed by autoimmune destruction, which generally is triggered by some environmental factor like a viral infection.

Initially there is gross lymphocytic infiltration in and around islets of Langerhans known as “insulitis”. The number and size of islets get reduced and later may be completely destroyed, which results in decreased insulin production and glucose intolerance and later stoppage of insulin production.

Several studies have suggested genetic basis in the development of type-1 diabetes and its pathogenesis. Generally some substances such as GAD (glutamic acid decarboxylase), IA-2, and incomplete forms of insulin start a false immune response, e.g. GAD and IA-2 are proteins that is present inside beta cells of islets of Langerhans, but rarely in certain circumstances they may leak out into the blood which prompt an immune attack against these proteins as body recognizes these as antigens and trigger an immune reaction against these. If beta cells are damaged insulin may leak out to blood stream in incomplete form which body recognizes as antigen and trigger an immune reaction against this incomplete form of insulin.

Type-2 Diabetes Pathogenesis:

In type-2 diabetes the beta cells of islets of Langerhans may be normal or slightly reduced in number or size and insulin production may be normal, slightly less or even higher than normal. The main feature of type-2 diabetes is the lack of sensitivity of muscle and fat cells to insulin or insulin resistance. More than normal insulin is produced to overcome the insulin resistance by the fat and muscle cells.

The insulin released by pancreas may also be abnormal or defective and cause increase in blood glucose level. Furthermore the live keeps producing glucose despite high glucose level in blood.