Effects of thyroid hormone on the gluconeogenic capacity of lipemic BHE rats.
Gluconeogenesis and ketogenesis from a variety of substrates by isolated hepatocytes from thyroxine-treated and control 40-hr starved BHE rats were determined. Thyroid hormone treatment stimulated glucose production from lactate and inhibited glucose production from alanine, lactate plus NH4Cl, or glutamate. beta-Hydroxybutyrate production by cells incubated with glycerol was decreased in the cells from thyroxine-treated rats. Glycerol had a greater antiketogenic effect in the thyroxine-treated rats than in the control rats. Acetoacetate production from 10:1 lactate:pyruvate, lactate plus NH4Cl, lactate plus lysine, and lactate plus ethanol was also less in the hepatocytes from the thyroxine-treated rats. Acetoacetate production from alanine was increased by thyroxine treatment. From these results it can be suggested that the metabolic abnormalities previously reported in the BHE rats can, in part, be attributable to abnormalities in endogenous thyroid hormone action and in part due to some as yet unknown regulatory process within the liver cell.
D000818:Animals; D005943:Gluconeogenesis / Q000187:drug effects*; D006949:Hyperlipidemias / Q000378:metabolism; D066298:In Vitro Techniques; D007700:Kinetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013974:Thyroxine / Q000494:pharmacology*
D013974:Thyroxine