INS and hyperinsulinism: It is possible that circulating higher levels of insulin in HC rats sustain the increased activities of MAPK, pp90rsk, PP-1, and glycogen synthase in the epididymal adipose tissue of HC rats and the reduced ability of insulin to further activate MAPK, PP-1, and glucose uptake above basal levels in adipocytes in HC rats may be a compensatory mechanism for the observed effects of chronic hyperinsulinemia in HC rats.