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胰岛素和胰高血糖素对泌乳大鼠乳腺脂肪生成的体内调节。胰岛素在转变为饥饿状态过程中的作用及作用位点。

Regulation of lactating-rat mammary-gland lipogenesis by insulin and glucagon in vivo. The role and site of action of insulin in the transition to the starved state.

作者信息

Jones R G, Ilic V, Williamson D H

出版信息

Biochem J. 1984 Oct 15;223(2):345-51. doi: 10.1042/bj2230345.

Abstract

Starvation for 6h and 24h caused an 80% and 95% decrease in the rate of mammary-gland lipogenesis respectively in conscious lactating rats. 2. Plasma insulin concentrations decreased and circulating ketone-body concentrations increased with the length of starvation. 3. The inhibition of lipogenesis after 24h starvation was accompanied by increased concentrations of glucose, glucose 6-phosphate and citrate in the mammary gland. Qualitatively similar changes were observed after 6h starvation. 4. Infusion of insulin at physiological concentrations caused a 100% increase in the rate of lipogenesis in fed animals and partially reversed the inhibition of lipogenesis caused by starvation. 5. Infusion of insulin tended to reverse the changes seen in intracellular metabolite concentrations. 4. Infusion of glucagon into fed rats caused no change in the rates of lipogenesis in mammary gland, liver or white adipose tissue. 7. It is concluded that (a) insulin acts physiologically to regulate lipogenesis in the mammary gland, (b) hexokinase and phosphofructokinase are important regulatory enzymes in the short-term control of lipogenesis in the mammary gland, which are under the influence of insulin, and (c) the unresponsiveness of mammary-gland lipogenesis in vivo to infusions of glucagon is consistent with an adaptive mechanism which diverts substrate towards the lactating mammary gland and away from other tissues.

摘要

在清醒的泌乳大鼠中,饥饿6小时和24小时分别导致乳腺脂肪生成率下降80%和95%。2. 血浆胰岛素浓度随着饥饿时间的延长而降低,循环酮体浓度则升高。3. 饥饿24小时后脂肪生成的抑制伴随着乳腺中葡萄糖、6-磷酸葡萄糖和柠檬酸浓度的增加。饥饿6小时后也观察到了定性相似的变化。4. 输注生理浓度的胰岛素使进食动物的脂肪生成率提高了100%,并部分逆转了饥饿引起的脂肪生成抑制。5. 输注胰岛素倾向于逆转细胞内代谢物浓度的变化。4. 向进食大鼠输注胰高血糖素对乳腺、肝脏或白色脂肪组织的脂肪生成率没有影响。7. 得出的结论是:(a) 胰岛素在生理上起作用以调节乳腺中的脂肪生成;(b) 己糖激酶和磷酸果糖激酶是乳腺脂肪生成短期控制中的重要调节酶,它们受胰岛素影响;(c) 乳腺脂肪生成在体内对输注胰高血糖素无反应,这与一种适应性机制一致,该机制将底物从其他组织转移到泌乳乳腺。

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