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胰岛素与甲状腺激素在脂肪生成调控中的相互作用。

Interactions between insulin and thyroid hormone in the control of lipogenesis.

作者信息

Sugden M C, Steare S E, Watts D I, Palmer T N

出版信息

Biochem J. 1983 Mar 15;210(3):937-44. doi: 10.1042/bj2100937.

Abstract
  1. The effects of intragastric glucose feeding and L-tri-iodothyronine (T3) administration on rates of hepatic and brown-fat lipogenesis in vivo were examined in fed and 48 h-starved rats. 2. T3 treatment increased hepatic lipogenesis in the fed but not the starved animals. Brown-fat lipogenesis was unaffected or slightly decreased by T3 treatment of fed or starved rats. 3. Intragastric glucose feeding increased hepatic lipogenesis in control or T3-treated fed rats, but did not increase hepatic lipogenesis in starved control rats. Glucose feeding increased hepatic lipogenesis if the starved rats were treated with T3. Glucose feeding increased rates of brown-fat lipogenesis in all experimental groups. The effects of glucose feeding on liver and brown-fat lipogenesis were mimicked by insulin injection. 4. The increase in hepatic lipogenesis in T3-treated 48 h-starved rats after intragastric glucose feeding was prevented by short-term insulin deficiency, but not by (-)-hydroxycitrate, an inhibitor of ATP citrate lyase. The increase in lipogenesis in brown adipose tissue in response to glucose feeding was inhibited by both short-term insulin deficiency and (-)-hydroxycitrate. 5. The results tend to preclude pyruvate kinase and acetyl-CoA carboxylase as the sites of interaction of insulin and T3 in the regulation of hepatic lipogenesis in 48 h-starved rats. Other potential sites of interaction are discussed.
摘要
  1. 研究了在喂食和饥饿48小时的大鼠体内,胃内输注葡萄糖和给予L-三碘甲状腺原氨酸(T3)对肝脏和棕色脂肪脂肪生成速率的影响。2. T3处理增加了喂食大鼠而非饥饿大鼠的肝脏脂肪生成。T3处理喂食或饥饿大鼠后,棕色脂肪脂肪生成未受影响或略有下降。3. 胃内输注葡萄糖增加了对照或T3处理的喂食大鼠的肝脏脂肪生成,但未增加饥饿对照大鼠的肝脏脂肪生成。如果饥饿大鼠用T3处理,葡萄糖输注会增加肝脏脂肪生成。葡萄糖输注增加了所有实验组的棕色脂肪脂肪生成速率。胰岛素注射模拟了葡萄糖输注对肝脏和棕色脂肪脂肪生成的影响。4. 胃内输注葡萄糖后,短期胰岛素缺乏可阻止T3处理的饥饿48小时大鼠肝脏脂肪生成的增加,但ATP柠檬酸裂解酶抑制剂(-)-羟基柠檬酸不能阻止。短期胰岛素缺乏和(-)-羟基柠檬酸均抑制了棕色脂肪组织对葡萄糖输注的脂肪生成增加。5. 这些结果倾向于排除丙酮酸激酶和乙酰辅酶A羧化酶作为胰岛素和T3在饥饿48小时大鼠肝脏脂肪生成调节中相互作用的位点。还讨论了其他潜在的相互作用位点。

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