Sugden M C, Holness M J
Department of Biochemistry, Faculty of Basic Medical Sciences, Queen Mary & Westfield College, University of London, UK.
FEBS Lett. 1993 Apr 26;321(2-3):121-6. doi: 10.1016/0014-5793(93)80091-8.
Despite significant increases in circulating concentrations of lipid fuels (triacylglycerol, non-esterified fatty acids (NEFA) and ketone bodies) in late-pregnant rats sampled in the fed (absorptive) state, cardiac and skeletal muscle active pyruvate dehydrogenase (PDHa) activities remained comparable with those observed in fed, age-matched virgin controls. Cardiac PDHa activity was suppressed in response to acute (6 h) starvation in late-pregnant (as well as virgin) rats: this inactivation was opposed by inhibition of mitochondrial long-chain FA oxidation. Starvation (6 h) also led to PDH inactivation in skeletal muscles of late-pregnant, but not virgin, rats. Starvation for 24 h led to further suppression of cardiac PDHa activity and was associated with significant increases in PDH kinase activities in both virgin and late-pregnant rats. Late pregnancy did not itself influence cardiac PDH kinase activity.
尽管在进食(吸收)状态下采样的妊娠晚期大鼠中,循环脂质燃料(三酰甘油、非酯化脂肪酸(NEFA)和酮体)浓度显著升高,但心脏和骨骼肌中活性丙酮酸脱氢酶(PDHa)的活性仍与年龄匹配的进食状态的未孕对照大鼠相当。妊娠晚期(以及未孕)大鼠急性饥饿(6小时)会抑制心脏PDHa活性:这种失活可通过抑制线粒体长链脂肪酸氧化来对抗。饥饿(6小时)也会导致妊娠晚期大鼠而非未孕大鼠骨骼肌中的PDH失活。饥饿24小时会导致心脏PDHa活性进一步受到抑制,并且与未孕和妊娠晚期大鼠中PDH激酶活性的显著增加有关。妊娠晚期本身并不影响心脏PDH激酶活性。