Hormonal regulation of ketogenesis in hepatocytes from fed rats before and after glycogen depletion.
Vasopressin, angiotensin II and the catecholamines decreased ketogenesis from oleate but increased ketogenesis from butyrate in hepatocytes from fed rats. The hormones increase CO2 production from both oleate and butyrate. It is suggested that whereas the mitochondrial uptake of butyrate is linked to its rate of oxidation, that of oleate is independent of its intramitochondrial metabolism, and consequently the oxidation of oleate to CO2 occurs at the expense of ketogenesis. Effects of the hormones on ketogenesis from oleate or butyrate were not observed after pre-treatment of the hepatocytes with dibutyryl cyclic AMP for 1 hour. The insensitivity of ketogenesis to the hormones after this treatment (which mimics the effects of acute carbohydrate deprivation in vivo) questions the physiological significance of hormonal regulation of ketogenesis other than at the onset of starvation.
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D002395:Catecholamines / Q000502:physiology; D000242:Cyclic AMP / Q000502:physiology; D005227:Fatty Acids / Q000378:metabolism; D007657:Ketone Bodies / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism*; D019301:Oleic Acid; D009829:Oleic Acids / Q000378:metabolism; D051381:Rats; D013329:Structure-Activity Relationship; D014667:Vasopressins / Q000502:physiology
D002395:Catecholamines; D005227:Fatty Acids; D007657:Ketone Bodies; D008112:Liver Glycogen; D009829:Oleic Acids; D014667:Vasopressins; D000804:Angiotensin II; D019301:Oleic Acid; D000242:Cyclic AMP