Differential effects of insulin, epinephrine, and glucagon on rat hepatocyte mitochondrial activity.
Oxidation of [2,3-14C]succinate carbons in the mitochondrial Krebs cycle was used as a probe to investigate the effects of insulin, epinephrine, glucagon, and 2,4-dinitrophenol (2,4-DNP) on isolated rat hepatocytes. Epinephrine, glucagon, and 2,4-DNP had a far greater stimulatory effect on 14CO2 formation from [2,3-14C]succinate than insulin. Unlike insulin, epinephrine and glucagon had no significant effect on the anabolic utilization of succinate carbons for protein synthesis. Our results suggest that although epinephrine, glucagon, and 2,4-DNP enhance the movement of tracer carbons through the Krebs cycle, only insulin is capable of enhancing amphibolite utilization for protein synthesis.
Mohan
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Department of Pharmacology and Nutrition, University of Southern California, School of Medicine, Los Angeles 90033.
Memon
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Bessman
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D019297:2,4-Dinitrophenol; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D002478:Cells, Cultured; D004140:Dinitrophenols / Q000494:pharmacology; D004837:Epinephrine / Q000502:physiology*; D005934:Glucagon / Q000502:physiology*; D007328:Insulin / Q000502:physiology*; D007700:Kinetics; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D051381:Rats; D011919:Rats, Inbred Strains; D013386:Succinates / Q000737:chemistry / Q000378:metabolism
D004140:Dinitrophenols; D007328:Insulin; D013386:Succinates; D002245:Carbon Dioxide; D005934:Glucagon; D019297:2,4-Dinitrophenol; D004837:Epinephrine