白桦脂酸通过抑制 3T3-L1 脂肪细胞中的胰岛素信号负调控因子和炎症激活蛋白激酶,改善 TNF-α 诱导的胰岛素抵抗。

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Hyun-Ah Lee, Jung-Kyung Lee, Ji-Sook Han
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引用次数: 0

摘要

背景:肥胖与胰岛素抵抗有关,而脂肪组织分泌的 TNF-α 可能在诱发肥胖方面发挥作用。TNF-α 可激活炎症蛋白激酶,损害胰岛素信号传导:材料与方法:3T3-L1 脂肪细胞在有或没有白桦脂酸的情况下暴露于 TNF-α。研究了葡萄糖摄取测定、细胞活力、参与胰岛素抵抗的蛋白质表达等各种参数:结果:白桦脂酸增加了 TNF-α 预处理细胞的葡萄糖摄取量,抑制了 PTP1B 和 JNK 的活化,减少了 IκBα 的降解。IRS-1中的酪氨酸磷酸化增加,丝氨酸磷酸化减少:讨论:白桦脂酸可恢复 TNF-α 受损的胰岛素信号传导,并增加 PI3K 的活化和 Akt 的磷酸化,增加 GLUT 4 的质膜表达,从而刺激葡萄糖摄取的浓度依赖性:这些结果表明,白桦脂酸可通过抑制胰岛素信号负调控因子和炎症激活蛋白激酶的活化,有效改善TNF-α诱导的脂肪细胞胰岛素抵抗,并有可能改善胰岛素抵抗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Betulinic acid improves TNF-α-induced insulin resistance by inhibiting negative regulator of insulin signalling and inflammation-activated protein kinase in 3T3-L1 adipocytes.

Context: Obesity is related to insulin resistance, and adipose tissue-secreted TNF-α may play a role in inducing obesity. TNF-α activates inflammatory protein kinase and impairs insulin signalling.

Objectives: We investigated the effect of betulinic acid on insulin resistance caused by TNF-α treatment in 3T3-L1 adipocytes.

Material and methods: 3T3-L1 was exposed to TNF-α in the presence and absence of betulinic acid. Various parameters such as glucose uptake assay, cell viability, expression of proteins involved in insulin resistance were studied.

Results: Betulinic acid increased glucose uptake in TNF-α pre-treated cells and inhibited the activation of PTP1B and JNK and reduced IκBα degradation. Tyrosine phosphorylation was increased, and serine phosphorylation was decreased in IRS-1.

Discussion: Betulinic acid restored TNF-α impaired insulin signalling and increased PI3K activation and phosphorylation of Akt and increased plasma membrane expression of GLUT 4, which stimulated glucose uptake concentration-dependently.

Conclusion: These results suggest that betulinic acid is effective at improving TNF-α-induced insulin resistance in adipocytes via inhibiting the activation of negative regulator of insulin signalling and inflammation-activated protein kinase and may potentially improve insulin resistance.

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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
期刊介绍: Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.
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