title: Metabolic fuel homeostasis in golden hamsters: effects of fasting, refeeding, glucose, and insulin.
abstract: Experiments were conducted to investigate possible metabolic correlates of the unusual ingestive behavior of hamsters after food deprivation. A hypothesis of metabolic refractoriness predicts that hamsters, unlike rats, should not show changes in plasma metabolic fuels, adipose tissue, or liver after fasting and subsequent refeeding. This hypothesis was discredited by findings that fasted hamsters, like rats, have increased plasma ketones and free fatty acids and decreased liver glycogen. On refeeding, hamsters showed rapid reversal of these changes, with supranormal glycogen content and apparent fatty acid synthesis in liver. Additional studies examined the metabolic responses of hamsters and rats to exogenous insulin or glucose administration. Incorporation of 3H2O into liver fatty acids was greatly elevated in rats by both insulin and glucose, but in hamsters only insulin was effective. Some of these metabolic differences may help our understanding of the unusual refractoriness of hamster food intake to various stimuli.
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D006224:Cricetinae; D004734:Energy Metabolism / Q000187:drug effects; D005215:Fasting; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D005502:Food; D005947:Glucose / Q000494:pharmacology*; D006706:Homeostasis; D007328:Insulin / Q000494:pharmacology*; D007659:Ketones / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism; D008297:Male; D008647:Mesocricetus; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D005227:Fatty Acids; D007328:Insulin; D007659:Ketones; D008112:Liver Glycogen; D005947:Glucose