Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway

doi:10.1038/s41598-024-68227-8

科研成果详情

题名	Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway
作者	Kaili Ye 1; Yanling Zhao2; Wen Huang2; Yonglin Zhu 3
发表日期	2024-08-01
发表期刊	Scientific Reports 影响因子和分区
语种	英语
原始文献类型	Journal Article
关键词	AMPK/Sirt1/PGC-1α signaling pathway Diabetic nephropathy Gut microbiota Short-chain fatty acids Sodium butyrate
其他关键词	CHAIN FATTY-ACIDS ; GLUCOSE-TOLERANCE ; GUT MICROBIOTA ; INFLAMMATION ; INHIBITION ; ACTIVATION ; CELLS ; FFA2
摘要	Diabetic nephropathy (DN) is a prototypical chronic energy metabolism imbalance disease. The AMPK/Sirt1/PGC-1α signaling pathway plays a pivotal role in regulating energy metabolism throughout the body. Gut microbiota ferment indigestible carbohydrates to produce a variety of metabolites, particularly short-chain fatty acids (SCFAs), which exert positive effects on energy metabolism. However, the potential for SCFAs to ameliorate DN-associated renal injury via the AMPK/Sirt1/PGC-1α pathway remains a matter of debate. In this study, we investigated the effects of sodium butyrate (NaB), a SCFA, on energy metabolism in mice with spontaneous DN at two different doses. Body weight, blood glucose and lipid levels, urinary protein excretion, liver and kidney function, interleukin-6 (IL-6) levels, and the expressions of AMPK, phosphorylated AMPK (p-AMPK), mitofusin 2 (MFN2), optic atrophy 1 (OPA1), and glucagon-like peptide-1 receptor (GLP-1R) were monitored in mice. Additionally, butyrate levels, gut microbiota composition, and diversity in colonic stool were also assessed. Our findings demonstrate that exogenous NaB supplementation can improve hyperglycemia and albuminuria, reduce renal tissue inflammation, inhibit extracellular matrix accumulation and glomerular hypertrophy, and could alter the gut microbiota composition in DN. Furthermore, NaB was found to upregulate the expressions of MFN2, OPA1, p-AMPK, and GLP-1R in DN renal tissue. These results suggest that NaB could improve the composition of gut microbiota in DN, activate the AMPK/Sirt1/PGC-1α signaling pathway, and enhance mitochondrial function to regulate energy metabolism throughout the body. Collectively, our findings indicate that NaB may be a novel therapeutic agent for the treatment of DN.
出版者	NATURE PORTFOLIO
ISSN	2045-2322
卷号	14 期号:1
DOI	10.1038/s41598-024-68227-8
页数	16
WOS类目	Multidisciplinary Sciences
WOS研究方向	Science & Technology - Other Topics
WOS记录号	WOS:001293364100039
收录类别	PUBMED ; SCIE ; SCOPUS
URL	查看原文
PubMed ID	39090182
SCOPUSEID	2-s2.0-85200255349
通讯作者地址	[Zhu, Yonglin]Wenzhou Med Univ, Wenzhou Peoples Hosp, Wenzhou Clin Inst 3, Dept Hematol, 299 Guan Rd,Louqiao St, Wenzhou 325000, Peoples R China.
Scopus学科分类	Multidisciplinary
SCOPUS_ID	SCOPUS_ID:85200255349
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/217100
专题	其他_温州市第三临床学院（温州市人民医院）附属第二医院附属第二医院_肾内科第二临床医学院、附属第二医院、育英儿童医院
作者单位	1.Department of Hematology of Wenzhou People's Hospital, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, No. 299, Guan Road, Louqiao Street, Ouhai District, Wenzhou, 325000, China.; 2.Department of Nephrology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.; 3.Department of Hematology of Wenzhou People's Hospital, The Wenzhou Third Clinical Institute Affiliated to Wenzhou Medical University, No. 299, Guan Road, Louqiao Street, Ouhai District, Wenzhou, 325000, China. qq1075540976@126.com.
第一作者单位	温州市第三临床学院（温州市人民医院）
通讯作者单位	温州市第三临床学院（温州市人民医院）
第一作者的第一单位	温州市第三临床学院（温州市人民医院）
推荐引用方式 GB/T 7714	Kaili Ye,Yanling Zhao,Wen Huang,et al. Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway[J]. Scientific Reports,2024,14(1).
APA	Kaili Ye, Yanling Zhao, Wen Huang, & Yonglin Zhu. (2024). Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway. Scientific Reports, 14(1).
MLA	Kaili Ye,et al."Sodium butyrate improves renal injury in diabetic nephropathy through AMPK/SIRT1/PGC-1α signaling pathway".Scientific Reports 14.1(2024).