GLYCOGEN-SYNTHASE ACTIVATION IN THE EPIDIDYMAL ADIPOSE-TISSUE FROM CHRONIC HYPERINSULINEMIC OBESE RATS/

Rat pups that received a high carbohydrate (HC) milk formula in their neonatal period became chronically hyperinsulinemic and obese in their adulthood. Pups born to HC female rats spontaneosly became chronicall y hyperinsulinemic and obese. Basal activities of mitogen-activated pr otein kinase (MAPK), 90-kD ribosomal S6 kinase (pp90(rsk)), protein ph osphatase-1 (PP-1), glycogen synthase, and protein kinase A (PKA) were measured in the epididymal adipose tissue of 100-day-old, male HC rat s (born to HC females) and compared with the activities in the epididy mal adipose tissue of rats born to mother-fed females (MF). Basal acti vities MAPK, pp90(rsk), PP-1, and glycogen synthase were increased in the epididymal adipose of HC rats while the basal activity of PKA was reduced. Insulin-stimulated activities of MAPK and PP-1 and glucose up take were also studied in adipocytes from these HC and MF rats. Althou gh the basal activities of MAPK and PP-1 and glucose uptake were highe r in adipocytes of HC rats, the ability of insulin to stimulate these processes in vitro above basal levels was less in these adipocytes com pared with adipocytes from MF rats. It is possible that circulating hi gher levels of insulin in HC rats sustain the increased activities of MAPK, pp90(rsk), PP-1, and glycogen synthase in the epididymal adipose tissue of HC rats and the reduced ability of insulin to further activ ate MAPK, PP-1, and glucose uptake above basal levels in adipocytes in HC mts may be a compensatory mechanism for the observed effects of ch ronic hyperinsulinemia in HC rats. (C) Elsevier Science Inc. 1998.