Diabetes & Insulin

By: Brandy Baggerly

Basic info on Diabetes

Insulin is a hormone released by pancreatic beta cells in response to elevated levels of nutrients in the blood. Insulin triggers the uptake of glucose, fatty acids and amino acids into the liver, adipose tissue and muscles and promotes the storage of these nutrients in the form of glycogen, lipids and proteins. Failure to uptake and store nutrients results in diabetes.

Type-1 diabetes is characterized by the inability to synthesize insulin, whereas in type-2 diabetes is when the body becomes resistant to the effects of insulin because of defects in the insulin signaling pathway.

Cell signaling pathway involved

In the insulin signal transduction pathway carbohydrates are consumed and the pancreas picks up on it, then there is a rise in blood glucose concentration and releases insulin O uptake from the blood stream. Insulin then binds to the insulin receptor which stores the glucose in the cell.The insulin receptor (IR) is a transmembrane receptor that is activated by the ligands insulin, IGF-I, IGF-II, which belongs to the large class of tyrosine kinase receptors.The binding of the ligand to the α-chains of the IR ectodomain makes structural changes in the receptor, leading to autophosphorylation of various tyrosine residues within the intracellular TK domain of the β-chain. These changes facilitate the recruitment of specific adapter proteins such as the insulin receptor substrate proteins (IRS) in addition to SH2-B(Src Homology 2 - B ), APS and protein phosphatases, such as PTP1B, eventually promoting downstream processes involving blood glucose homeostasis.

Correct mechanism of diabetes

In the correct mechanism of diabetes the pathways will signal correctly and mitogen will activate protein kinases. The interaction via kinases will not be coupled to IRS proteins.

Current direction of diabetes research

Research toward a cure is focused on transplantation of the cells in the pancreas that produce insulin, the islet cells or parts of the pancreas. In type 1 diabetes, the body’s immune system turns on itself and destroys these islet cells. As a result, the body doesn't produce the insulin required to escort glucose from the food we eat to where it is needed. Research is now focusing on ways to understand this immune attack to find safe ways to block it. There are many ongoing studies using knowledge of immunology to try to intervene and prevent type 1 diabetes. Diabetes investigators are working on understanding how islet cells malfunction in type 2 diabetes. Some questions being researched includes "What is the genetic basis for this? Why can islets in some people continue to compensate by making more and more insulin for many years without getting diabetes, whereas others can’t keep up with the increased demand?".