Abstract
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 spontaneously became chronically hyperinsulinemic and obese. Basal activities of mitogen-activated protein kinase (MAPK), 90-kD ribosomal S6 kinase (pp90 rsk), protein phosphatase-1 (PP-1), glycogen synthase, and protein kinase A (PKA) were measured in the epididymal adipose tissue of 100-day-old male HC rats (born to HC females) and compared with the activities in the epididymal adipose tissue of rats born to mother-fed females (MF). Basal activities of 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 uptake were also studied in adipocytes from these HC and MF rats. Although the basal activities of MAPK and PP-1 and glucose uptake were higher in adipocytes of HC rats, the ability of insulin to stimulate these processes in vitro above basal levels was less in these adipocytes compared with adipocytes from MF rats. It is possible that circulating higher 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 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.
Published Version
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