Enhanced hepatic insulin sensitivity and peripheral glucose uptake in cold acclimating rats.
Cold-exposed rats exhibit hypermetabolism, hyperphagia, and increased glucose oxidation. Their counterregulatory hormone secretion is markedly elevated, while insulin levels fall acutely, gradually returning to basal during acclimation. We assessed both hepatic and peripheral sensitivity to insulin in rats in the basal state and after 5 days of cold (5 C) exposure. The contribution of gluconeogenesis to total glucose turnover was measured and compared to daily urinary corticosterone excretion. Hepatic glucose production was equally suppressed by the infusion of insulin at 1.2 mU/kg X min in both control and cold-acclimated rats, but enhanced hepatic sensitivity to low dose (0.6 mU/kg X min) insulin infusion was only observed after cold exposure. The metabolic clearance of glucose was elevated with cold stress and was insensitive to the infusion of insulin at either level. Insulin resistance was not observed. Urinary excretion of corticosterone and urea nitrogen were markedly increased, but creatinine excretion was unchanged, suggesting that the concurrent increase in gluconeogenesis resulted from increased protein intake rather than increased catabolism of muscle protein.
D000222:Adaptation, Physiological; D000818:Animals; D001806:Blood Urea Nitrogen; D001835:Body Weight; D003080:Cold Temperature; D003345:Corticosterone / Q000652:urine; D005947:Glucose / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D007700:Kinetics; D008099:Liver / Q000187:drug effects*; D008297:Male; D008657:Metabolic Clearance Rate; D008954:Models, Biological; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D005947:Glucose; D003345:Corticosterone