Han HF, Liu SZ, Zhang X, Wei M, Huang X, Yu WB. Duodenal-jejunal bypass increases intraduodenal bile acids and upregulates duodenal SIRT1 expression in high-fat diet and streptozotocin-induced diabetic rats. World J Gastroenterol 2022; 28(31): 4338-4350 [PMID: 36159018 DOI: 10.3748/wjg.v28.i31.4338]
Corresponding Author of This Article
Wen-Bin Yu, MD, PhD, Chief Doctor, Professor, Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, No. 107 West Wenhua Road, Jinan 250012, Shandong Province, China. wenbin_yu2003@163.com
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Basic Study
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Han HF, Liu SZ, Zhang X, Wei M, Huang X, Yu WB. Duodenal-jejunal bypass increases intraduodenal bile acids and upregulates duodenal SIRT1 expression in high-fat diet and streptozotocin-induced diabetic rats. World J Gastroenterol 2022; 28(31): 4338-4350 [PMID: 36159018 DOI: 10.3748/wjg.v28.i31.4338]
World J Gastroenterol. Aug 21, 2022; 28(31): 4338-4350 Published online Aug 21, 2022. doi: 10.3748/wjg.v28.i31.4338
Duodenal-jejunal bypass increases intraduodenal bile acids and upregulates duodenal SIRT1 expression in high-fat diet and streptozotocin-induced diabetic rats
Hai-Feng Han, Shao-Zhuang Liu, Xiang Zhang, Meng Wei, Xin Huang, Wen-Bin Yu, Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, Shandong Province, China
Author contributions: Han HF and Yu WB conceived of the experiments; Liu SZ and Yu WB designed the experiments; Han HF, Zhang X, Wei M, and Huang X carried out the experiments, performed the statistical analyses and wrote the manuscript; and all authors have commented on the initial and final drafts of the manuscript and approved the final version of the article.
Supported bythe National Natural Science Foundation of China, No. 81600617, 81700708, 81702647 and 82100853; and the Natural Science Foundation of Shandong Province, No. ZR2020MH246, ZR2021LZL003 and ZR2021QH028.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care Committee of Cheeloo College of Medicine, Shandong University, (Protocol No. 19085).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Corresponding author: Wen-Bin Yu, MD, PhD, Chief Doctor, Professor, Department of General Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, No. 107 West Wenhua Road, Jinan 250012, Shandong Province, China. wenbin_yu2003@163.com
Received: May 26, 2022 Peer-review started: May 26, 2022 First decision: June 19, 2022 Revised: June 28, 2022 Accepted: July 25, 2022 Article in press: July 25, 2022 Published online: August 21, 2022 Processing time: 82 Days and 2.6 Hours
Core Tip
Core Tip: The intrinsic mechanisms of diabetes remission after duodenal-jejunal bypass (DJB) surgery are complicated. Duodenal SIRT1 is a novel therapeutic target for diabetes, and increased duodenal SIRT1 is linked to improved hepatic insulin sensitivity and decreased hepatic glucose output. The animal study demonstrated that DJB increased intraduodenal bile acid (BA) levels, activated the BA signaling pathway, and upregulated SIRT1 expression in the duodenal mucosa. Our cell experiments proved that farnesoid X receptor and Takeda G-protein-coupled receptor 5 activation increased SIRT1 expression in rat small intestine epithelial cells, indicating that increased intraluminal BAs and activation of BA receptors contributed to increased duodenal SIRT1 after DJB.
