The administration of a low-carbohydrate\high-saturated-fat (LC\HF) diet for 28 days or starvation for 48 h both increased pyruvate dehydrogenase kinase (PDHK) activity in extracts of rat hepatic mitochondria, by approx. 2.1-fold and 3.5-fold respectively. ELISAs of extracts of hepatic mitochondria, conducted over a range of pyruvate dehydrogenase (PDH) activities, revealed that mitochondrial immunoreactive PDHKII (the major PDHK isoform in rat liver) was significantly increased by approx. 1.4-fold after 28 days of LC\HF feeding and by approx. 2-fold after 48 h of starvation. The effect of LC\HF feeding to increase hepatic PDHK activity was retained through hepatocyte preparation, but was decreased on 21 h culture with insulin (100 µ-i.u.\ml). A sustained (24 h) 2-4-fold elevation in plasma insulin concentration in i o (achieved by insulin infusion via an osmotic pump) suppressed the effect of LC\HF feeding so that hepatic
Antibodies to purified recombinant PDHKII were used for ELISAs of PDHKII in mitochondrial extracts. In liver, hyperthyroidism elicited a 2.3-fold increase in PDHK activity (7'<0.01) which was accompanied by a significant 1.5-fold (P < 0.001) increase in the amount of mitochondrial immunoreactive PDHKII. In contrast, despite a stable 2.0-fold increase in cardiac PDHK activity (P < 0.001), the amount of mitochondrial immunoreactive PDHKII in heart was unaffected by hyperthyroidism. The mechanisms for long-term regulation of PDHK activity by thyroid hormones therefore differ fundamentally between heart and liver.
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