Effects of glucagon and insulin on fatty acid synthesis and glycogen degradation in the perfused liver of normal and genetically obese (ob/ob) mice
| Autor: | D A Hems, Gary Y. Ma, C D Gove |
|---|---|
| Rok vydání: | 1978 |
| Předmět: |
endocrine system
medicine.medical_specialty Glycogenolysis Vasopressins medicine.medical_treatment Mice Obese Biology Carbohydrate metabolism Biochemistry Glucagon Mice chemistry.chemical_compound Internal medicine Lipid biosynthesis medicine Animals Insulin Molecular Biology Fatty acid synthesis chemistry.chemical_classification Glycogen Fatty Acids digestive oral and skin physiology Fatty acid Cell Biology Liver Glycogen Glucose Endocrinology Liver chemistry Female hormones hormone substitutes and hormone antagonists Research Article Acetyl-CoA Carboxylase |
| Zdroj: | Biochemical Journal. 174:761-768 |
| ISSN: | 0264-6021 |
| DOI: | 10.1042/bj1740761 |
| Popis: | 1. Rapid effects of hormones on glycogen metabolism and fatty acid synthesis in the perfused liver of the mouse were studied. 2. In perfusions lasting 2h, of livers from normal mice, glucagon in successive doses, each producing concentrations of 10(-10) or 10(-9)M, inhibited fatty acid and cholesterol synthesis. In perfusions lasting 40–50 min, in which medium was not recycled, inhibition of fatty acid synthesis was only observed with glucagon at concentrations greater than 10(-9)M. This concentration was about two orders of magnitude higher than that required for the stimulation of glycogen breakdown. Glucagon did not inhibit the activity of acetyl-CoA carboxylase, assayed 10 or 20 min after addition of glucagon (10(-9) or 10(-10)M). It is proposed that the action of glucagon on hepatic fatty acid biosynthesis could be secondary in time to depletion of glycogen. Insulin prevented the effect of glucagon (10(-10)M) on glycogenolysis, but not that of vasopressin. 3. Livers of genetically obese (ob/ob) mice did not show significant inhibition of lipid biosynthesis in response to glucagon, although there was normal acceleration of glycogen breakdown. This resistance to glucagon action was not reversed by food deprivation. Livers of obese mice exhibited resistance to the counteraction by insulin of glucagon-stimulated glycogenolysis, which was reversible by partial food deprivation. |
| Databáze: | OpenAIRE |
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