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Brown adipocyte mineralocorticoid receptor deficiency impairs metabolic regulation in diet-induced obese mice

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机构： [1]Department of Clinical Laboratory Medicine, Guangdong Provincial Key Laboratory of Major Obstetric Diseases [2]Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology [3]The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. [4]Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People’s Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [5]National Center for Stomatology [6]National Clinical Research Center for Oral Diseases [7]Shanghai Key Laboratory of Stomatology, Shanghai, China. [8]Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [9]Department of Oncology, Guangzhou Geriatric Hospital, Guangzhou, China. [10]Department of infectious diseases, Renmin Hospital of Wuhan University, Wuhan, China. [11]Department of Clinical Medicine, The Third Clinical School of Guangzhou Medical University, Guangzhou, China. [12]Guangzhou Key Laboratory for Clinical Rapid Diagnosis and Early Warning of Infectious Diseases, King Med School of Laboratory Medicine, Guangzhou Medical University, Guangzhou, China. [13]Department of Teaching management, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. [14]Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Shanghai, China

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Activation of brown adipose tissue (BAT) contributes to energy dissipation and metabolic health. Although mineralocorticoid receptor (MR) antagonists have been demonstrated to improve metabolism under obesity, the underlying mechanisms remain incompletely understood. We aimed to evaluate the role of BAT MR in metabolic regulation. After 8 weeks of high fat diet (HFD) feeding, BAT MR knockout (BMRKO) mice manifested significantly increased body weight, fat mass, serum fasting glucose and impaired glucose homeostasis compared to littermate control (LC) mice, although insulin resistance and fasting serum insulin were not significantly changed. Metabolic cage experiments showed no change in O2 consumption, CO2 production or energy expenditure in obese BMRKO mice. RNA sequencing analysis revealed downregulation of genes related to fatty acid metabolism in BAT of BMRKO-HFD mice compared to LC-HFD mice. Moreover, H&E and immunohistochemical staining demonstrated that BMRKO exacerbated HFD-induced macrophage infiltration and pro-inflammatory genes in epididymal white adipose tissue (eWAT). BMRKO-HFD mice also manifested significantly increased liver weights and hepatic lipid accumulation, an increasing trend of genes related to lipogenesis and lipid uptake, and significantly decreased genes related to lipolytic and fatty acid oxidation in the liver. Finally, the level of insulin-induced AKT phosphorylation was substantially blunted in eWAT, but not liver or skeletal muscle of BMRKO-HFD mice compared to LC-HFD mice. These data suggest that BAT MR is required to maintain metabolic homeostasis, likely through its regulation of fatty acid metabolism in BAT and impacts on eWAT and liver.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

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出版当年[2022]版：

大类 | 2 区生物学

小类 | 2 区生化与分子生物学

最新[2025]版：

大类 | 2 区医学

小类 | 2 区生化与分子生物学

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出版当年[2021]版：

Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

最新[2023]版：

Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

影响因子： 5 最新[2023版] 5.7 最新五年平均 6.676 出版当年[2021版] 6.656 出版当年五年平均 5.922 出版前一年[2020版] 6.5 出版后一年[2022版]

第一作者：

第一作者机构： [1]Department of Clinical Laboratory Medicine, Guangdong Provincial Key Laboratory of Major Obstetric Diseases [2]Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology [3]The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. [4]Laboratory of Oral Microbiota and Systemic Diseases, Shanghai Ninth People’s Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

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通讯作者：

通讯机构： [1]Department of Clinical Laboratory Medicine, Guangdong Provincial Key Laboratory of Major Obstetric Diseases [2]Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology [3]The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. [6]National Clinical Research Center for Oral Diseases [7]Shanghai Key Laboratory of Stomatology, Shanghai, China. [8]Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [9]Department of Oncology, Guangzhou Geriatric Hospital, Guangzhou, China. [10]Department of infectious diseases, Renmin Hospital of Wuhan University, Wuhan, China. [*1]Department of infectious diseases, Renmin Hospital of Wuhan University, Wuhan,China [*2]Department of Clinical Laboratory Medicine, Guangdong Provincial Key Laboratory of Major Obstetric Diseases ,Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology ,The Third Affiliated Hospital of Guangzhou Medical University, No. 63, Duobao Road, Liwan District, Guangzhou City, 510150, China [*3]Shanghai Ninth People's Hospital Research Center, Shanghai Jiao Tong University School of Medicine, 115 Jinzun Rd, Shanghai, 200125, China.

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