Transport and metabolism of fructose in fat cells of normal and hypophysectomized rats.
We have shown earlier that the glucose carrier of fat cells of hypophysectomized rats operates at maximal speed in the basal state and that these cells are insensitive to insulin. Here we characterize fructose transport and metabolism in adipocytes of normal and hypophysectomized rats. 3-O-methylglucose inhibits insulin-stimulated incorporation of [U-14C]fructose into fat cells and has no significant effect on basal fructose metabolism. In contrast, 2-deoxyglucose inhibits both basal and insulin-stimulated fructose incorporation. Insulin enhances fructose incorporation in normal adipocytes only in the absence of 3-O-methylglucose. In hypophysectomized rats, incorporation of glucose and of fructose is decreased and insensitive to insulin. In contrast to the glucose carrier, the specific fructose carrier appears to be insensitive to insulin and to continue to operate with unchanged characteristics after hypophysectomy. Thus, hypophysectomy leads to a specific alteration of the insulin-sensitive glucose carrier, whereas the insulin-insensitive fructose carrier remains unaltered.
D000273:Adipose Tissue / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D005632:Fructose / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D008297:Male; D010902:Pituitary Gland / Q000502:physiology*; D051381:Rats; D014284:Triiodothyronine / Q000494:pharmacology
D014284:Triiodothyronine; D005632:Fructose; D000324:Adrenocorticotropic Hormone; D005947:Glucose