Holness M J, French T J, Schofield P S, Sugden M C
Department of Chemical Pathology, London Hospital Medical College, U.K.
Biochem J. 1987 Nov 1;247(3):621-6. doi: 10.1042/bj2470621.
The administration of glucose to 48 h-starved euthyroid or hyperthyroid rats led to decreased blood concentrations of fatty acids and ketone bodies in both groups, but fatty acid concentrations were higher and ketone-body concentrations lower in the latter group. Decreased ketonaemia was not due to increased ketone-body clearance. Flux through carnitine palmitoyltransferase 1 was increased, consistent with the effects of hyperthyroidism on enzyme activity demonstrated in vitro. Correlations between the concentrations of ketone bodies and long-chain acylcarnitine measured in freeze-clamped liver samples indicated that a lower proportion of the product of beta-oxidation was used for ketone-body synthesis. Citrate concentrations were unaffected by hyperthyroidism, but lipogenesis was increased. The results are discussed in relation to the factors controlling hepatic carbon flux and energy requirements after re-feeding.
对饥饿48小时的正常甲状腺或甲状腺功能亢进大鼠给予葡萄糖后,两组大鼠的血液中脂肪酸和酮体浓度均降低,但后一组的脂肪酸浓度较高,酮体浓度较低。酮血症降低并非由于酮体清除增加所致。肉碱棕榈酰转移酶1的通量增加,这与甲状腺功能亢进对体外所证实的酶活性的影响一致。在冷冻钳夹的肝脏样本中测得的酮体浓度与长链酰基肉碱浓度之间的相关性表明,β氧化产物用于酮体合成的比例较低。柠檬酸浓度不受甲状腺功能亢进的影响,但脂肪生成增加。结合再喂养后控制肝脏碳通量和能量需求的因素对结果进行了讨论。