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Different mechanisms underlie the long‐term regulation of pyruvate dehydrogenase kinase (PDHK) by tri‐iodothyronine in heart and liver
Author(s) -
Priestman David A,
Donald Elaine,
Holness Mark J,
Sugden Mary C
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)01430-0
Subject(s) - medicine , endocrinology , pyruvate dehydrogenase complex , hormone , pyruvate kinase , mitochondrion , pyruvate dehydrogenase kinase , biology , chemistry , biochemistry , enzyme , metabolism , glycolysis
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.