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GATA-3 作为胰岛素抵抗和 2 型糖尿病的潜在治疗靶点。

GATA-3 as a Potential Therapeutic Target for Insulin Resistance and Type 2 Diabetes Mellitus.

机构信息

Biomedical Research Center, Qatar University, Doha, Qatar.

出版信息

Curr Diabetes Rev. 2021;17(2):169-179. doi: 10.2174/1573399816666200705210417.

DOI:10.2174/1573399816666200705210417
PMID:32628587
Abstract

Impaired adipogenesis plays an important role in the development of obesity-associated insulin resistance and type 2 diabetes as it leads to ectopic fat deposition. The anti-adipogenic transcription factor GATA-3 was identified as one of the potential molecular targets responsible for the impairment of adipogenesis. The expression of GATA-3 is higher in insulinresistant obese individuals compared to BMI-matched insulin-sensitive counterparts. Adipose tissue inflammation is a crucial mediator of this process. Hyperglycemia mediates the activation of the immune system, partially through upregulation of GATA- 3, causing exacerbation of the inflammatory state associated with obesity. This review discusses the evidence supporting the inhibition of GATA-3 as a useful therapeutic strategy in obesity-associated insulin resistance and type 2 diabetes, through up-regulation adipogenesis and amelioration of the immune response.

摘要

脂肪生成受损在肥胖相关胰岛素抵抗和 2 型糖尿病的发展中起着重要作用,因为它会导致异位脂肪沉积。抗脂肪生成转录因子 GATA-3 被确定为导致脂肪生成受损的潜在分子靶点之一。与 BMI 匹配的胰岛素敏感对照组相比,胰岛素抵抗肥胖个体中的 GATA-3 表达更高。脂肪组织炎症是该过程的关键介质。高血糖通过上调 GATA-3 部分介导免疫系统的激活,导致与肥胖相关的炎症状态恶化。这篇综述讨论了支持抑制 GATA-3 作为肥胖相关胰岛素抵抗和 2 型糖尿病的一种有用治疗策略的证据,通过上调脂肪生成和改善免疫反应。

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