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脂肪组织可塑性与2型糖尿病发病机制中的胰岛素信号传导

Adipose Tissue Plasticity and Insulin Signaling in the Pathogenesis of Type 2 Diabetes.

作者信息

Sakaguchi Masaji

机构信息

Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuoku, Kumamoto 860-8556 Japan.

出版信息

Diabetol Int. 2023 Dec 18;15(1):28-33. doi: 10.1007/s13340-023-00676-4. eCollection 2024 Jan.

Abstract

Obesity is a major cause of various metabolic disorders, including type 2 diabetes, nonalcoholic fatty liver disease (NAFLD) and cardiovascular diseases, in modern times. Fat tissue originally evolved as an organ to prepare for food shortages. However, when individuals consume excessive calories and engage in insufficient physical activity, it can lead to the excessive accumulation of lipids in white adipose tissue, potentially causing problems. In response to this excessive lipid accumulation extending to other tissues, insulin resistance is triggered in the body as a physiological response to prevent harmful effects. Additionally, in mammals, brown adipose tissue has evolved to generate energy and maintain body temperature. These inconspicuous defense mechanisms function coordinately to protect against systemic metabolic abnormalities affecting multiple organs. Understanding the dynamic nature of adipose tissues is now crucial for elucidating the details of the molecular abnormalities in obesity-associated metabolic diseases. This review outlines adipocyte plasticity and function with a focus on the physiological relevance and new pathways of insulin signaling.

摘要

肥胖是现代各种代谢紊乱的主要原因,包括2型糖尿病、非酒精性脂肪性肝病(NAFLD)和心血管疾病。脂肪组织最初作为一种器官进化而来,以应对食物短缺。然而,当个体摄入过多热量且身体活动不足时,会导致白色脂肪组织中脂质过度积累,从而可能引发问题。作为一种生理反应,为防止有害影响,身体会在这种过度脂质积累扩展到其他组织时触发胰岛素抵抗。此外,在哺乳动物中,棕色脂肪组织已进化到可产生能量并维持体温。这些不显眼的防御机制协同发挥作用,以防止影响多个器官的全身性代谢异常。了解脂肪组织的动态特性对于阐明肥胖相关代谢疾病中分子异常的细节至关重要。本综述概述了脂肪细胞的可塑性和功能,重点关注胰岛素信号传导的生理相关性和新途径。

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