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胰岛素对分化的ob17脂肪样细胞中脂质合成酶的调节作用。

Modulation of lipid-synthesizing enzymes by insulin in differentiated ob17 adipose-like cells.

作者信息

Grimaldi P, Forest C, Poli P, Negrel R, Ailhaud G

出版信息

Biochem J. 1983 Aug 15;214(2):443-9. doi: 10.1042/bj2140443.

Abstract

ob17 cells convert into adipose-like cells when maintained in the presence of physiological concentrations of insulin and tri-iodothyronine. After this conversion, insulin removal from differentiated ob17 cells gives within 24-48 h a large decrease in fatty acid synthetase, glycerol 3-phosphate dehydrogenase and acid:CoA ligase activities, as well as in the rate of fatty acid synthesis determined by [14C]acetate incorporation into lipids. All parameters are restored by insulin addition to initial values within 24-48 h. Dose-response curves of insulin on the restoration of glycerol 3-phosphate dehydrogenase activity and of fatty acid synthesis give half-maximally effective concentrations close to 1 nM, in agreement with the affinity for insulin of the insulin receptors previously characterized in these cells. Immunotitration experiments indicate that the changes in the specific activity of fatty acid synthetase are due to parallel changes in the cellular enzyme content. Therefore the ob17 cell line should be a useful model to study the long-term effects of insulin on the modulation of lipid synthesis in adipose cells.

摘要

当在生理浓度的胰岛素和三碘甲状腺原氨酸存在的情况下培养时,ob17细胞会转化为脂肪样细胞。这种转化后,从分化的ob17细胞中去除胰岛素会在24 - 48小时内使脂肪酸合成酶、3 - 磷酸甘油脱氢酶和酰基辅酶A连接酶的活性大幅下降,以及由[14C]乙酸掺入脂质所测定的脂肪酸合成速率大幅下降。在24 - 48小时内,通过添加胰岛素,所有参数都能恢复到初始值。胰岛素对3 - 磷酸甘油脱氢酶活性恢复和脂肪酸合成的剂量反应曲线给出的半最大有效浓度接近1 nM,这与先前在这些细胞中表征的胰岛素受体对胰岛素的亲和力一致。免疫滴定实验表明,脂肪酸合成酶比活性的变化是由于细胞酶含量的平行变化。因此,ob17细胞系应该是研究胰岛素对脂肪细胞脂质合成调节的长期影响的有用模型。

相似文献

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Insulin and lipogenesis in rat adipocytes. I. Effect of insulin incubation on lipid synthesis by isolated rat adipocytes.
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The effect of triiodothyronine on fatty acid synthetase activity and content in differentiating ob17 preadipocytes.
Biochim Biophys Acta. 1983 Feb 7;750(2):282-90. doi: 10.1016/0005-2760(83)90030-9.

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