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TGR5-Mediated Bile Acid Sensing Controls Glucose Homeostasis
Open accessAbstract
TGR5 is a G protein-coupled receptor expressed in brown adipose tissue and muscle, where its activation by bile acids triggers an increase in energy expenditure and attenuates diet-induced obesity. Using a combination of pharmacological and genetic gain- and loss-of-function studies in vivo, we show here that TGR5 signaling induces intestinal glucagon-like peptide-1 (GLP-1) release, leading to improved liver and pancreatic function and enhanced glucose tolerance in obese mice. In addition, we show that the induction of GLP-1 release in enteroendocrine cells by 6alpha-ethyl-23(S)-methyl-cholic acid (EMCA, INT-777), a specific TGR5 agonist, is linked to an increase of the intracellular ATP/ADP ratio and a subsequent rise in intracellular calcium mobilization. Altogether, these data show that the TGR5 signaling pathway is critical in regulating intestinal GLP-1 secretion in vivo, and suggest that pharmacological targeting of TGR5 may constitute a promising incretin-based strategy for the treatment of diabesity and associated metabolic disorders.
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In the citing paper
“Bacteria-derived secondary bile acids (lithocholic acid, deoxycholic acid) can activate the G-protein coupled bile acid receptor Gpbar1 receptor (TGR5) in L cells, promoting the peripheral release of GLP-1 and PYY (Katsuma et al., 2005;Thomas et al., 2009;Ullmer et al., 2013).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Thomas et al., 2009
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In the citing paper
“Bile acids also increase energy expenditure in brown adipose tissue, preventing obesity and resistance to insulin. This effect is dependent on induction of the type 2 iodothyronine deiodinase and is mediated by the binding of bile acids to a novel G-protein-coupled receptor TGR5 148.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [148]
In the citing paper
“Bile acids induce insulin secretion directly via the transmembrane bile acid receptor Takeda G protein–coupled receptor 5 (on β cells and indirectly via stimulation of l-cell derived GLP-1 and subsequent insulin release (110–112).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [112]
In the citing paper
“TGR5 is therefore a new and attractive target for treating obesity, since it can theoretically protect against obesity and its complications via two distinct and potentially synergistic mechanisms: increased energy expenditure and improved insulin sensitivity 148.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [148]
In the citing paper
“Bile acids also increase energy expenditure in brown adipose tissue, preventing obesity and resistance to insulin. This effect is dependent on induction of the type 2 iodothyronine deiodinase and is mediated by the binding of bile acids to a novel G-protein-coupled receptor TGR5 148.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [148]
In the citing paper
“One promising TGR5 agonist, INT-777, has already shown efficacy in vivo, increasing energy expenditure and reducing adiposity in mice with diet-induced obesity 148,149.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [148]
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Citations
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Metadata
- Authors
- Thomas, C., Gioiello, A., Noriega, L., Strehle, A., Oury, J., Rizzo, G., Macchiarulo, A., Yamamoto, H., Mataki, C., Pruzanski, M., Pellicciari, R., Auwerx, J., & Schoonjans, K.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- University of Perugia (IT)
- Intercept Pharmaceuticals (United States) (US)
- Corresponding author
- Auwerx, Johan
- Schoonjans, Kristina
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2009-09
- Volume
- 10
- Issue
- 3
- Pages
- 167-177
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC2739652
- OpenAlex
- W2081271380
- Cited by
- 1,885
- References
- 43
- Citations by year
- 2026: 143 · 2025: 100 · 2024: 153 · 2023: 112 · 2022: 135 · 2021: 141 · 2020: 148 · 2019: 113 · 2018: 124 · 2017: 126 · 2016: 106 · 2015: 108 · 2014: 87 · 2013: 91 · 2012: 69
- FWCI
- 47.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1415 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- Institut National de la Santé et de la Recherche Médicale
- European Commission
- Centre National de la Recherche Scientifique
- Australian Research Council
- National Institutes of Health
- Agence Nationale de la Recherche
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
- Keywords
- TGR5, glucose homeostasis, glucagon-like peptide-1, enteroendocrine cells, energy expenditure, diet-induced obesity, diabesity, ATP/ADP ratio, calcium mobilization, brown adipose tissue, pancreatic function, liver function, TGR5 agonists, INT-777, incretin-based therapy
- MeSH terms
- Adenosine Triphosphate, Animals, Bile Acids and Salts, Calcium, Cell Line, Cholic Acids, Cricetulus, Glucose, Cricetinae, Homeostasis, Humans, Insulin, Male, Mice, Inbred C57BL, Mice, Obese, Oxidative Phosphorylation, Signal Transduction, CHO Cells, Mice, Knockout, Enteroendocrine Cells, Receptors, G-Protein-Coupled, Mice, Glucagon-Like Peptide 1
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