I have a hypothesis that explains how T2DM develops in a more convincing order. I think that the human body when exposed to excessive glucose enters a storage mode, the mirror image of starvation mode. When too much carbs are ingested an insulin spike ensues leading to sending new deposits of fat to the visceral stores. The body intentionally raises its insulin level
In order to cling to the newly stored visceral fat. Such increase is met by down regulating muscles' s insulin receptors to avoid hypoglycaemia. So IR develops as a physiological adaptation to remain in the storage mode. Now mankind is accustomed to cycling starvation and storage periods while in our days the storage mode continues permanently leading to another adaptation. The pancreas, after most of the fat cells are full, decreases its secretion of insulin to avoid pathogenic depositing of fat. It keeps lowering insulin, which remains relatively high, until the insulin is not sufficient to drive the glucose from the blood to the muscles. And it's Diabetes.
In order to cling to the newly stored visceral fat. Such increase is met by down regulating muscles' s insulin receptors to avoid hypoglycaemia. So IR develops as a physiological adaptation to remain in the storage mode. Now mankind is accustomed to cycling starvation and storage periods while in our days the storage mode continues permanently leading to another adaptation. The pancreas, after most of the fat cells are full, decreases its secretion of insulin to avoid pathogenic depositing of fat. It keeps lowering insulin, which remains relatively high, until the insulin is not sufficient to drive the glucose from the blood to the muscles. And it's Diabetes.
