Masashi Kobayashi

TL;DR: In severely diabetic, catabolic animals, insulin binding to receptors is increased due to enhanced receptor capacity and affinity; in mildly diabetic rats only receptor capacity is increased; glucose transport activity and intracellular pathways of glucose metabolism are impaired in insulin-deficient diabetic animals, most likely due to hypoinsulinemia.

TL;DR: Insulin isolated from the pancreas of a diabetic patient with fasting hyperinsulinaemia showed decreased activity in binding to cell membrane insulin receptors and in stimulating cellular 2-deoxyglucose transport and glucose oxidation.

TL;DR: The results suggested that pioglitazone increased insulin sensitivity in part by activating kinase of the receptors through indirect effect on insulin receptors and that the drug may have useful benefits in insulin resistance of NIDDM.

TL;DR: Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, it is concluded that this patient's insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system.

TL;DR: The impaired biologic activity of this patient's circulating insulin was probably due to a structural abnormality and fortuitously obtained from his pancreas during a laparotomy for a pancreatic cyst.