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司美格鲁肽对肥胖诱导的肾脏疾病及肥胖诱导的肾透明细胞癌的保护作用

Protective Effect of Semaglutide on Obesity-Induced Renal Disease and Obesity-Induced Kidney Renal Clear Cell Carcinoma.

作者信息

Wang Shuqi, Zhang Mengmeng, Yang Xiaoman, Chen Shuchun

机构信息

Department of Internal Medicine, Hebei Medical University, Shijiazhuang, People's Republic of China.

Department of Endocrinology, Hebei General Hospital, Shijiazhuang, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2025 Mar 19;18:805-818. doi: 10.2147/DMSO.S498447. eCollection 2025.

DOI:10.2147/DMSO.S498447
PMID:40124099
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11930019/
Abstract

PURPOSE

Proteomics was used to study the effect of semaglutide on the expression of renal protein in obese mice, and looking for proteins that could improve the prognosis of Kidney Renal Clear Cell Carcinoma (KIRC).

MATERIALS AND METHODS

Thirty-six mice were randomly divided into normal-fat diet group (NFD), high-fat diet group (HFD), high-fat diet plus semaglutide intervention group (HS). Collected mice serum, urine, kidney tissue samples, and detected urinary protein/creatinine, blood glucose, blood lipid, inflammation, oxidative stress and other related indicators. Different staining methods were used to analyze the pathological changes of mice's kidneys. Liquid chromatography-tandem mass spectrometry mass spectrometry (LC-MS/MS) analysis was used to analyze the total protein in the kidneys of mice. Finally, bioinformatics technology was used to analyze significantly different expressed proteins (DEPs).

RESULTS

The mechanism of semaglutide protecting the kidneys were related to oxidative phosphorylation, PPAR signaling pathway, thiamine, butyric acid and tryptophan metabolism pathways. Moreover, semaglutide could significantly increase the expression of Man1a1 and Ntn4 in the kidneys of mice, while the high-expression of Man1a1 and Ntn4 in KIRC population had a better overall survival rate.

CONCLUSION

Semaglutide could regulate the development of KIRC by up-adjusting the expression of Man1a1 and Ntn4.

摘要

目的

采用蛋白质组学研究司美格鲁肽对肥胖小鼠肾脏蛋白质表达的影响，寻找可改善肾透明细胞癌（KIRC）预后的蛋白质。

材料与方法

将36只小鼠随机分为正常脂肪饮食组（NFD）、高脂饮食组（HFD）、高脂饮食加司美格鲁肽干预组（HS）。收集小鼠血清、尿液、肾脏组织样本，检测尿蛋白/肌酐、血糖、血脂、炎症、氧化应激等相关指标。采用不同染色方法分析小鼠肾脏的病理变化。运用液相色谱-串联质谱（LC-MS/MS）分析小鼠肾脏中的总蛋白。最后，利用生物信息学技术分析差异显著的表达蛋白（DEPs）。

结果

司美格鲁肽保护肾脏的机制与氧化磷酸化、PPAR信号通路、硫胺素、丁酸和色氨酸代谢途径有关。此外，司美格鲁肽可显著增加小鼠肾脏中Man1a1和Ntn4的表达，而KIRC人群中Man1a1和Ntn4的高表达具有更好的总生存率。

结论

司美格鲁肽可通过上调Man1a1和Ntn4的表达来调节KIRC的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/092391edc4c8/DMSO-18-805-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/65e279912f9a/DMSO-18-805-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/1a9358ebbc08/DMSO-18-805-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/20c2b1e76ee1/DMSO-18-805-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/82c50a1627de/DMSO-18-805-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/092391edc4c8/DMSO-18-805-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/65e279912f9a/DMSO-18-805-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/1a9358ebbc08/DMSO-18-805-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/20c2b1e76ee1/DMSO-18-805-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/82c50a1627de/DMSO-18-805-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0884/11930019/092391edc4c8/DMSO-18-805-g0005.jpg

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