Insulin represses CYP/PXR activation by transport of the transcription factor FOXO1 out of the nucleous. No porphyrogenic metabolic effects.

Antidiabetic pancreatic hormone consisting of two polypeptide chains, A and B, connected by two diulphide bridges.

Used in the treatment of diabetes mellitus. Rapid, short changes in the energy flow of the body are controlled by insulin, glucagon and catecholamines. Long term effects are mediated by glucocorticoides, growth hormone and thyroid hormones. Pancreatic release of insulin and glucagon are inversely controlled by the blood glucose levels. Insulin is liberated from the beta cells in response to increased concentration of glucose in blood. It lowers the blood glucose level by inhibition of gluconeogenesis and hepatic glycogenolysis, by increase in glycogen synthesis in the liver, and by accelerating muscle and fat depot uptake of glucose. In fatty tissue the uptake of triglyceride from blood is augmented via activation of lipoprotein lipase, but attenuated in muscle and heart. The net effect of the insulin response is increased energy production via glucose oxidation and decreased FA oxidation. Through nuclear export of the active transcription factor FOXO1. The activation pressure on PXR/CAR is attenuated.

Many observations on safe use.

Uneventful use reported in 3 patients with acute porphyria. In total there are 19 reports of uneventful use of different types of insulin.