The Relationship between Metabolic State and Total CoA Content of Rat Liver and Heart

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Abstract
An insulin-glucagon directed regulation of CoA levels in liver was suggested by in vivo experiments comparing levels of total CoA (unacylated plus acylated CoA) in alloxan-diabetic versus control rats, and by comparing total CoA contents of rats at various stages of a meal-feeding schedule. The liver total CoA of alloxan-diabetic rats was 1.9 times greater (nmoles/g wet weight) than controls, and liver mitochondrial total CoA was 1.6 times greater (nmoles/mg protein). Rats on a meal-feeding schedule killed 2 or 4 hours after the meal had total CoA contents 28% and 40% lower, respectively, than 21-hour fasted rats, and liver mitochondrial total CoA contents 15% and 28% lower. Comparisons of pantothenate and cyst(e)ine2 contents in these livers suggested that the total CoA level was not regulated via influx of precursors. The liver pantothenate was equal in alloxan-diabetic rats and controls, although fasted rats had significantly higher levels of liver pantothenate than fed rats. The liver cyst(e)ine content was not changed by feeding. The heart maintained a higher pantothenate level than liver (36 and 11.3 nmoles/g wet weight for heart and liver of control rats, respectively) and a lower total CoA content (138 vs. 288 nmoles/g wet weight for heart and liver, respectively). However, heart total CoA was not changed by alloxan-induced diabetes or by feeding. Comparison of total CoA, unacylated CoASH, and acylated CoA contents in livers of meal-fed rats suggested that a limitation of CoA availability in the fasted state was prevented by increases in the total CoA content.