Nurjahan Nurjhan

TL;DR: Metformin acts primarily by decreasing hepatic glucose output, largely by inhibiting gluconeogenesis, and also seems to induce weight loss, preferentially involving adipose tissue.

TL;DR: It is concluded that increased gluconeogenesis is the predominant mechanism responsible for increased hepatic glucose output in NIDDM.

TL;DR: It is concluded that increased substrate delivery to the liver and increased efficiency of intrahepatic substrate conversion to glucose are both important factors for the increased gluconeogenesis of NIDDM and that tissues other than muscle are responsible for the increase delivery of gluconeogenic precursors to the Liver.

TL;DR: It is concluded that lipolysis is increased in NIDDM and, although more glycerol is thus available, increased activity of the intrahepatic pathway for conversion of glycericol into glucose, due at least in part to increased plasma free fatty acids, is the predominant mechanism responsible for enhanced glycersol gluconeogenesis.

TL;DR: In normal humans there is an autoregulatory process independent of changes in plasma glucose and glucoregulation hormone concentrations which prevents a substrate-induced increase in gluconeogenesis from increasing overall hepatic glucose output; since this process cannot be explained on the basis of inhibition of gluc oneogenesis from other substrates, it probably involves diminution of glycogenolysis.