Different mechanisms underlie the long‐term regulation of pyruvate dehydrogenase kinase (PDHK) by tri‐iodothyronine in heart and liver
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 (P<0.01) which was accompanied by a significant 1.5‐fold (P<0.001) increase in the amount of mitochondrial immunor...
| Main Authors: | , , , |
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| 格式: | Journal article |
| 出版: |
Wiley
1997
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| 總結: | 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 (P<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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