Endocrine Abstracts

Case reports in humans implicate glucocorticoid (GC) excess, through exogenous administration or endogenous overproduction, as a cause of non-alcoholic fatty liver disease. In rodents, massive doses of GCs have induced fatty liver when liver fat was measured in the fasting state. The mechanisms through which GCs might induce fatty liver are unknown, but are thought to be secondary to insulin resistance/hyperinsulinaemia. In this study, we examined the effect of dexamethasone (...

Background: In mice, a methionine-choline deficient diet (MCDD) causes steatohepatitis and hepatic insulin resistance. In contrast, a simple choline-deficient diet (CDD) causes liver fat accumulation without steatohepatitis, insulin resistance or weight loss. We hypothesised that differences in liver and adipose fatty acid metabolism underlie the contrasting predisposition to steatohepatitis and hepatic insulin resistance.Methods: C57Bl6 mice (male, aged...

Background: GCs retard growth prenatally in many mammals. Little is known of the prenatal effects of GCs in mice though this species is optimal for genetic and transgenic studies. IGFBP-2 is the predominant prenatal IGF binding protein and it may influence IGF action.Aim: To determine the weights, crown rump lengths (CRL) and serum IGF-I, Insulin and IGFBP-2 levels on 1 day old mice exposed to GC prenatally.Methods: Pregnant mice w...