Abstract
In order to elucidate the pathogenesis of transient glucose intolerance in acute hepatitis, we measured serum immunoreactive insulin (IRI) during 100g-OGTT in 31 cases of acute hepatitis, of which insulin sensitivity index (ISI) was calculated 7 cases during acute stage and after recovery. The number of cases in which 125I-insulin specific binding to circulating mononuclear cells was measured in acute and recovery stage were 8 and 5 cases, respectively. During acute stage, BS and IRI were increased, whereas the peripheral insulin activity (A), defined as a peripheral insulin resistance and ISI were decreased. After recovery, BS, A and ISI returned to almost nomal value. Insulin binding was significantly decreased (0.34±0.06%) (M±SEM) during acute stage, compared with normals (1.03±0.57%) (p<0.01). However, it returned to normal (1.01±0.58%), after recovery. Scatchard plots revealed that its decrease in acute stage was mainly due to reduced binding site per cell. From these results, we conclude that the reduced insulin recepter may play significant role for the pathogenesis of transient glucose intolerance in acute hepatitis.
