PMID- 32309446 OWN - NLM STAT- MEDLINE DCOM- 20210216 LR - 20220414 IS - 2314-6753 (Electronic) IS - 2314-6745 (Print) VI - 2020 DP - 2020 TI - Roux-en-Y Gastric Bypass in Obese Diabetic Rats Promotes Autophagy to Improve Lipid Metabolism through mTOR/p70S6K Signaling Pathway. PG - 4326549 LID - 10.1155/2020/4326549 [doi] LID - 4326549 AB - PURPOSE: To investigate the effects of Roux-en-Y gastric bypass (RYGB) surgery on markers of liver mitochondrial dynamics and find new therapeutic basis on obese type 2 diabetes mellitus (T2DM) patients. Materials and Methods. Thirty-two rats were divided into nondiabetic group, diabetic group, sham group, and RYGB group. The Dual-energy X-ray absorptiometry (DEXA) was used to detect short-term curriculum vitae for rat body component and fat and lean mass. Hepatic lipid content and triglyceride levels were detected by Oil Red O staining. Western blotting was used to examine autophagy and mammalian target of rapamycin/P70S6 kinase (mTOR/p70S6K) pathway-related proteins. The carbon dioxide production from the oxidation of [(14)C] oleate was measured. Plasma glucose was measured by glucose oxidase assay. The insulin and C-peptide were detected. Triacylglyceride (TG) and free fat acid (FFA) in plasma were determined by enzymatic colorimetric assays. RESULTS: RYGB improved metabolic parameters and enhanced plasma GLP-1 level, ameliorated the lipopexia, and increased insulin sensitivity in the liver; RYGB promoted the hepatic autophagy and inhibited the mTOR/p70S6K signaling pathway. GLP-1 reduced fat load and increased fatty acid beta-oxidation by activated autophagy to regulate the hepatic lipid pathway through mTOR/p70S6K signaling pathway. CONCLUSIONS: RYGB may reduce liver lipid toxicity and improve insulin sensitivity through activating the hepatic fat hydrolysis pathway and inhibiting the liver fat synthesis pathway. However, the transport pathway of liver fat does not play a key role. CI - Copyright (c) 2020 Nanxi Ma et al. FAU - Ma, Nanxi AU - Ma N AD - Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China. FAU - Ma, Rui AU - Ma R AD - Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China. FAU - Tang, Kaixin AU - Tang K AD - Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China. FAU - Li, Xuesong AU - Li X AD - Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China. FAU - He, Bing AU - He B AUID- ORCID: 0000-0002-9694-6591 AD - Department of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China. LA - eng PT - Journal Article DEP - 20200326 PL - England TA - J Diabetes Res JT - Journal of diabetes research JID - 101605237 RN - 0 (Blood Glucose) RN - 89750-14-1 (Glucagon-Like Peptide 1) RN - EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Animals MH - Autophagy/*physiology MH - Blood Glucose/metabolism MH - Diabetes Mellitus, Experimental/metabolism/*surgery MH - *Gastric Bypass MH - Glucagon-Like Peptide 1/blood MH - Insulin Resistance/physiology MH - Lipid Metabolism/*physiology MH - Male MH - Obesity/metabolism/*surgery MH - Rats MH - Rats, Sprague-Dawley MH - Ribosomal Protein S6 Kinases, 70-kDa/*metabolism MH - Signal Transduction/*physiology MH - TOR Serine-Threonine Kinases/*metabolism PMC - PMC7136782 COIS- The authors declare that they have no competing interests. EDAT- 2020/04/21 06:00 MHDA- 2021/02/17 06:00 PMCR- 2020/03/26 CRDT- 2020/04/21 06:00 PHST- 2019/10/10 00:00 [received] PHST- 2020/01/28 00:00 [revised] PHST- 2020/02/12 00:00 [accepted] PHST- 2020/04/21 06:00 [entrez] PHST- 2020/04/21 06:00 [pubmed] PHST- 2021/02/17 06:00 [medline] PHST- 2020/03/26 00:00 [pmc-release] AID - 10.1155/2020/4326549 [doi] PST - epublish SO - J Diabetes Res. 2020 Mar 26;2020:4326549. doi: 10.1155/2020/4326549. eCollection 2020.