Takeda G Protein-Coupled Receptor 5-Mechanistic Target of Rapamycin Complex 1 Signaling Contributes to the Increment of Glucagon-Like Peptide-1 Production after Roux-en-Y Gastric Bypass
The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings. Circulating bile acids...
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| Published in | EBioMedicine Vol. 32; pp. 201 - 214 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.06.2018
Elsevier |
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| Online Access | Get full text |
| ISSN | 2352-3964 2352-3964 |
| DOI | 10.1016/j.ebiom.2018.05.026 |
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| Abstract | The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings.
Circulating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB.
Positive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells.
Deoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB.
•Ileal mTORC1 signaling activity and GLP-1 production are up-regulated by RYGB in both rodents and human subjects.•Manipulation of intestinal mTORC1 signaling alters the up-regulation of GLP-1 induced by RYGB.•Ileal TGR5-mTORC1 signaling and GLP-1 production are positively correlative with plasma deoxycholic acid in mice.•Deoxycholic acid enhances synthesis and secretion of GLP-1 through TGR5-mTORC1 pathway in STC-1 cells.
Diabetes resolves rapidly after RYGB. GLP-1 improves glycemic control in rodents and patients. Although literature has documented that postprandial secretion of GLP-1 is enhanced after RYGB, its underlying molecular mechanisms remain poorly understood. We have identified the deoxycholic acid-TGR5-mTORC1 signaling pathway as a potential mechanism by which RYGB increases GLP-1 production, thus expanding its interest as a target for the treatment of type 2 diabetes mellitus. |
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| AbstractList | The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings.
Circulating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB.
Positive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells.
Deoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB.
•Ileal mTORC1 signaling activity and GLP-1 production are up-regulated by RYGB in both rodents and human subjects.•Manipulation of intestinal mTORC1 signaling alters the up-regulation of GLP-1 induced by RYGB.•Ileal TGR5-mTORC1 signaling and GLP-1 production are positively correlative with plasma deoxycholic acid in mice.•Deoxycholic acid enhances synthesis and secretion of GLP-1 through TGR5-mTORC1 pathway in STC-1 cells.
Diabetes resolves rapidly after RYGB. GLP-1 improves glycemic control in rodents and patients. Although literature has documented that postprandial secretion of GLP-1 is enhanced after RYGB, its underlying molecular mechanisms remain poorly understood. We have identified the deoxycholic acid-TGR5-mTORC1 signaling pathway as a potential mechanism by which RYGB increases GLP-1 production, thus expanding its interest as a target for the treatment of type 2 diabetes mellitus. Background: The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings. Methods: Circulating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB. Results: Positive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells. Interpretation: Deoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB. Keywords: Deoxycholic acid, GLP-1, mTORC1, RYGB, TGR5 The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings.BACKGROUNDThe mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings.Circulating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB.METHODSCirculating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB.Positive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells.RESULTSPositive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells.Deoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB.INTERPRETATIONDeoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB. The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings. Circulating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB. Positive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells. Deoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB. AbstractBackgroundThe mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we investigated whether TGR5-mTORC1 signaling mediates the RYGB-induced alteration in GLP-1 production in mice and human beings. MethodsCirculating bile acids, TGR5-mTORC1 signaling, GLP-1 synthesis and secretion were determined in lean or obese male C57BL/6 mice with or without RYGB operation, as well as in normal glycemic subjects, obese patients with type 2 diabetes before and after RYGB. ResultsPositive relationships were observed among circulating bile acids, ileal mechanistic target of rapamycin complex 1 (mTORC1) signaling and GLP-1 during changes in energy status in the present study. RYGB increased circulating bile acids, ileal Takeda G protein-coupled receptor 5 (TGR5) and mTORC1 signaling activity, as well as GLP-1 production in both mice and human subjects. Inhibition of ileal mTORC1 signaling by rapamycin significantly attenuated the stimulation of bile acid secretion, TGR5 expression and GLP-1 synthesis induced by RYGB in lean and diet-induced obese mice. GLP-1 production and ileal TGR5-mTORC1 signaling were positively correlated with plasma deoxycholic acid (DCA) in mice. Treatment of STC-1 cells with DCA stimulated the production of GLP-1. This effect was associated with a significant enhancement of TGR5-mTORC1 signaling. siRNA knockdown of mTORC1 or TGR5 abolished the enhancement of GLP-1 synthesis induced by DCA. DCA increased interaction between mTOR-regulatory-associated protein of mechanistic target of rapamycin (Raptor) and TGR5 in STC-1 cells. InterpretationDeoxycholic acid-TGR5-mTORC1 signaling contributes to the up-regulation of GLP-1 production after RYGB. • Ileal mTORC1 signaling activity and GLP-1 production are up-regulated by RYGB in both rodents and human subjects. • Manipulation of intestinal mTORC1 signaling alters the up-regulation of GLP-1 induced by RYGB. • Ileal TGR5-mTORC1 signaling and GLP-1 production are positively correlative with plasma deoxycholic acid in mice. • Deoxycholic acid enhances synthesis and secretion of GLP-1 through TGR5-mTORC1 pathway in STC-1 cells. Diabetes resolves rapidly after RYGB. GLP-1 improves glycemic control in rodents and patients. Although literature has documented that postprandial secretion of GLP-1 is enhanced after RYGB, its underlying molecular mechanisms remain poorly understood. We have identified the deoxycholic acid-TGR5-mTORC1 signaling pathway as a potential mechanism by which RYGB increases GLP-1 production, thus expanding its interest as a target for the treatment of type 2 diabetes mellitus. |
| Author | Xu, Geyang Li, Hanbing Huang, Zhaoqi Qin, Tingfeng Zhai, Hening Zhang, Weizhen Li, Zhi Zhang, Heng Peng, Miao Chen, Linxi |
| AuthorAffiliation | c Shenzhen University Diabetes Center, Shenzhen University Health Science Center, Shenzhen, Guangdong 518060, China d Department of Surgery, University of Michigan Medical Center, Ann Arbor, MI 48109-0346, USA b Endoscopy Center, The First Affiliated Hospital of Jinan University, 613 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510630, China a Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China |
| AuthorAffiliation_xml | – name: a Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – name: d Department of Surgery, University of Michigan Medical Center, Ann Arbor, MI 48109-0346, USA – name: c Shenzhen University Diabetes Center, Shenzhen University Health Science Center, Shenzhen, Guangdong 518060, China – name: b Endoscopy Center, The First Affiliated Hospital of Jinan University, 613 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510630, China |
| Author_xml | – sequence: 1 givenname: Hening surname: Zhai fullname: Zhai, Hening organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 2 givenname: Zhi surname: Li fullname: Li, Zhi organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 3 givenname: Miao surname: Peng fullname: Peng, Miao organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 4 givenname: Zhaoqi surname: Huang fullname: Huang, Zhaoqi organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 5 givenname: Tingfeng surname: Qin fullname: Qin, Tingfeng organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 6 givenname: Linxi surname: Chen fullname: Chen, Linxi organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 7 givenname: Hanbing surname: Li fullname: Li, Hanbing organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 8 givenname: Heng surname: Zhang fullname: Zhang, Heng organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China – sequence: 9 givenname: Weizhen surname: Zhang fullname: Zhang, Weizhen email: weizhenz@umich.edu organization: Shenzhen University Diabetes Center, Shenzhen University Health Science Center, Shenzhen, Guangdong 518060, China – sequence: 10 givenname: Geyang surname: Xu fullname: Xu, Geyang email: xugeyangliang@163.com organization: Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29859856$$D View this record in MEDLINE/PubMed |
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| Keywords | FXR DCA GLP-1 S6 RYGB ip Raptor S6K1 Deoxycholic acid TGR5 BAs mTOR Cyp7a1 mTORC1 Farnesoid X receptor Roux-en-Y gastric bypass mechanistic target of rapamycin Intraperitoneal Ribosomal protein subunit 6 kinase 1 Takeda G protein-coupled receptor 5 Bile acids Regulatory-associated protein of mechanistic target of rapamycin Cytochrome P450 family 7 subfamily A member 1 Ribosomal protein S6 Glucagon-like peptide-1 mechanistic target of rapamycin complex 1 |
| Language | English |
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| Snippet | The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined. Here we... AbstractBackgroundThe mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely... • Ileal mTORC1 signaling activity and GLP-1 production are up-regulated by RYGB in both rodents and human subjects. • Manipulation of intestinal mTORC1... Background: The mechanism by which Roux-en-Y Gastric Bypass (RYGB) increases the secretion of glucagon-like peptide-1 (GLP-1) remains incompletely defined.... |
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| SubjectTerms | Advanced Basic Science Animals Bile Acids and Salts - blood Blood Glucose Deoxycholic acid Deoxycholic Acid - blood Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - surgery Gastric Bypass - adverse effects Gene Expression Regulation - genetics GLP-1 Glucagon-Like Peptide 1 - biosynthesis Glucagon-Like Peptide 1 - genetics Humans Insulin Resistance - genetics Internal Medicine Male Mechanistic Target of Rapamycin Complex 1 - genetics Mice Mice, Obese Middle Aged mTORC1 Obesity - blood Obesity - genetics Obesity - pathology Obesity - surgery Receptors, G-Protein-Coupled - genetics Research Paper RYGB Signal Transduction - genetics TGR5 |
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| Title | Takeda G Protein-Coupled Receptor 5-Mechanistic Target of Rapamycin Complex 1 Signaling Contributes to the Increment of Glucagon-Like Peptide-1 Production after Roux-en-Y Gastric Bypass |
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