Insulin sensitivity in experimental cirrhosis.

To investigate insulin action in muscle and adipose tissue in hepatic cirrhosis, a recently described animal model was used. Dimethylnitrosamine administration induced histologically proven cirrhosis. Contrary to expectation, muscle strips from cirrhotic rats displayed increased insulin sensitivity both with respect to glycogen synthesis (ED50 0.11 +/- 0.01 vs 0.23 +/- 0.04 nmol/l; p less than 0.03) and glucose oxidation (ED50 0.36 +/- 0.07 vs 0.97 +/- 12 nmol/l; p less than 0.02). As the cirrhotic rats had failed to gain weight normally, it is postulated that a state of relative starvation accounted for the enhanced insulin sensitivity. These data demonstrate that the severe insulin resistance characteristically associated with cirrhosis is reversible. Control of nutritional state in future studies upon DMNA induced cirrhosis should permit detailed examination of the cellular mechanisms controlling insulin sensitivity in hepatic cirrhosis.