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缺乏改善了高脂饮食诱导的小鼠肥胖，并改善了其新陈代谢。

deficiency ameliorates high-fat diet-induced obesity and improves metabolism in mice.

作者信息

Duan Sirui, Li Bo, Cui Shiyu, Chen Yaoyao, He Ying, Fan Lihong

机构信息

Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Department of Cardiology, Ninth Hospital of Xi'an, Xi'an, China.

出版信息

Front Nutr. 2024 May 9;11:1387806. doi: 10.3389/fnut.2024.1387806. eCollection 2024.

DOI:10.3389/fnut.2024.1387806
PMID:38784133
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11111939/
Abstract

OBJECTIVE

Obesity is defined as excess body fat and is a current health epidemic associated with increased risk for type 2 diabetes and cardiovascular disease. The ClC-3 chloride channel/antiporter, encoded by the , is associated with some diseases, like carcinoma, nervous system diseases, and metabolic diseases. To verify the relationship between the and weight including metabolic changes, searching for a new target for metabolic therapy of obesity, we designed the experiment.

METHODS

The mice were divided into 4 different groups: mice + high-fat diet (HFD), mice + HFD, mice + normal diet (ND), mice + ND, and fed for 16 weeks. After the glucose tolerance test and insulin tolerance test, peripheral blood and adipose tissues were collected. Moreover, we performed transcriptome sequencing for the epididymal white adipose tissue from and mice with the high-fat diet. Western blotting verified the changes in protein levels of relevant metabolic genes.

RESULTS

We found that the mice had lower body weight and visceral fat, refining glucose and lipid metabolism in HFD-induced mice, but had no effect in normal diet mice. RNA-seq and Western blotting indicated that deficiency may inhibit obesity through the AMPK-UCP1 axis.

CONCLUSION

Modulation of may provide an appealing therapeutic target for obesity and associated metabolic syndrome.

摘要

目的

肥胖被定义为体内脂肪过多，是当前一种与2型糖尿病和心血管疾病风险增加相关的健康流行病。由[基因名称]编码的ClC-3氯通道/反向转运体与某些疾病相关，如癌症、神经系统疾病和代谢性疾病。为了验证[基因名称]与体重之间的关系，包括代谢变化，寻找肥胖代谢治疗的新靶点，我们设计了本实验。

方法

将小鼠分为4组：[基因敲除小鼠] + 高脂饮食（HFD）组、[野生型小鼠] + HFD组、[基因敲除小鼠] + 正常饮食（ND）组、[野生型小鼠] + ND组，并喂养16周。在进行葡萄糖耐量试验和胰岛素耐量试验后，采集外周血和脂肪组织。此外，我们对高脂饮食的[基因敲除小鼠]和[野生型小鼠]的附睾白色脂肪组织进行了转录组测序。蛋白质印迹法验证了相关代谢基因蛋白水平的变化。

结果

我们发现[基因敲除小鼠]体重和内脏脂肪较低，改善了高脂饮食诱导小鼠的糖脂代谢，但对正常饮食小鼠没有影响。RNA测序和蛋白质印迹表明，[基因名称]缺陷可能通过AMPK-UCP1轴抑制肥胖。

结论

调节[基因名称]可能为肥胖及相关代谢综合征提供一个有吸引力的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/f7ec0e2256dc/fnut-11-1387806-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/ded38b0d6fa5/fnut-11-1387806-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/5fca86bfa1d8/fnut-11-1387806-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/954a7ef8de94/fnut-11-1387806-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/dfd8370e28b3/fnut-11-1387806-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/ba6e7a280054/fnut-11-1387806-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/f7ec0e2256dc/fnut-11-1387806-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/ded38b0d6fa5/fnut-11-1387806-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/5fca86bfa1d8/fnut-11-1387806-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/954a7ef8de94/fnut-11-1387806-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/dfd8370e28b3/fnut-11-1387806-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/ba6e7a280054/fnut-11-1387806-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05e3/11111939/f7ec0e2256dc/fnut-11-1387806-g006.jpg

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