Insulin receptor
Also known as: INSR, insulin receptor tyrosine kinase
The receptor on muscle, fat and liver cells through which insulin moves glucose out of the blood and into storage. Insulin injections act on it directly in type 1 diabetes; in type 2 diabetes the receptor's signalling is blunted (insulin resistance) and metformin helps restore the response.
- Kind
- receptor
- Also called
- INSR, insulin receptor tyrosine kinase
- Where it is found
- Cell membranes of skeletal muscle, fat, liver and most other tissues, including the brain.
What it does
Insulin from the pancreatic beta cells binds the outer part of its receptor, a tyrosine kinase that spans the cell membrane, and the receptor phosphorylates itself and a chain of signalling proteins inside the cell. In muscle and fat the signal brings GLUT4 glucose transporters to the cell surface, so glucose floods in and is burned or stored as glycogen and fat; in the liver it switches off glucose production and switches on glycogen and fat synthesis; in all tissues it promotes protein synthesis and blocks the breakdown of fat. In type 1 diabetes the beta cells are destroyed and injected insulin, in rapid- and long-acting forms, replaces the hormone; in type 2 diabetes the receptors are present but the signal is dampened by excess fat inside cells and by inflammation, so the pancreas overproduces insulin until it can no longer keep up. Weight loss, exercise and metformin improve the receptor response; sulfonylureas and GLP-1 agonists increase insulin supply. The main danger of insulin treatment is hypoglycaemia when the dose exceeds the food and activity of the day.
Role in the body
Uptake and storage of glucose, suppression of hepatic glucose output, promotion of protein and fat synthesis; growth signalling.