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[亮氨酸B24]胰岛素和[亮氨酸B25]胰岛素不是脂肪细胞中脂肪生成的拮抗剂。

[LeuB24]- and [LeuB25]insulins are not antagonists of lipogenesis in adipocytes.

作者信息

Diaconescu C, Saunders D, Gattner H G, Brandenburg D

出版信息

Hoppe Seylers Z Physiol Chem. 1982 Feb;363(2):187-92. doi: 10.1515/bchm2.1982.363.1.187.

Abstract

Semisynthetic human [LeuB24]-and [LeuB25]insulins were investigated to determine whether they show antagonistic properties towards insulin-stimulated lipogenesis in isolated fat cells. In contrast to other reports, we could detect only an additive agonistic effect when constant concentrations (e.g. 0.3 ng/ml) of the analogues were mixed with varying concentrations of insulin, or when constant concentrations (e.g. 0.3 ng/ml, 0.6 ng/ml) of insulin were mixed with varying concentrations of the analogues. Similar results were obtained with mixtures of insulin and NA2-acetyl- or NA2-propionyl-des-GlyA1-insulins. These results do not support the contention that a diabetic state could be caused by either of these mutant human insulins.

摘要

研究了半合成人[亮氨酸B24]-和[亮氨酸B25]胰岛素,以确定它们对分离脂肪细胞中胰岛素刺激的脂肪生成是否具有拮抗特性。与其他报告相反,当将恒定浓度(例如0.3 ng/ml)的类似物与不同浓度的胰岛素混合时,或者当将恒定浓度(例如0.3 ng/ml、0.6 ng/ml)的胰岛素与不同浓度的类似物混合时,我们仅能检测到相加激动作用。胰岛素与NA2-乙酰基-或NA2-丙酰基-去甘氨酸A1-胰岛素的混合物也得到了类似结果。这些结果不支持这些突变型人胰岛素中的任何一种可导致糖尿病状态的观点。

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