The DOI matches its Crossref record; 255 of the 255 references it cites were found in a registry or an index.
Bile acids and bariatric surgery
Open accessAbstract
Bariatric surgery, specifically Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG), are the most effective and durable treatments for morbid obesity and potentially a viable treatment for type 2 diabetes (T2D). The resolution rate of T2D following these procedures is between 40 and 80% and far surpasses that achieved by medical management alone. The molecular basis for this improvement is not entirely understood, but has been attributed in part to the altered enterohepatic circulation of bile acids. In this review we highlight how bile acids potentially contribute to improved lipid and glucose homeostasis, insulin sensitivity and energy expenditure after these procedures. The impact of altered bile acid levels in enterohepatic circulation is also associated with changes in gut microflora, which may further contribute to some of these beneficial effects. We highlight the beneficial effects of experimental surgical procedures in rodents that alter bile secretory flow without gastric restriction or altering nutrient flow. This information suggests a role for bile acids beyond dietary fat emulsification in altering whole body glucose and lipid metabolism strongly, and also suggests emerging roles for the activation of the bile acid receptors farnesoid x receptor (FXR) and G-protein coupled bile acid receptor (TGR5) in these improvements. The limitations of rodent studies and the current state of our understanding is reviewed and the potential effects of bile acids mediating the short- and long-term metabolic improvements after bariatric surgery is critically examined.
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“Looking for the next step in obesity pharmacotherapies, the concept of combining entero-pancreatic hormones for obesity treatment was supported by the marked WL, sustained weight maintenance, and metabolic benefits observed with BS, which increase multiple gut hormone levels [9–14].”
From Triple Agonism Based Therapies for Obesity (2025) · cites this paper as [14]
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Role of bile acids in metabolic control
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Mechanisms of Weight Loss After Obesity Surgery
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Triple Agonism Based Therapies for Obesity
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Metadata
- Authors
- Albaugh, V. L., Banan, B., Ajouz, H., Abumrad, N. N., & Flynn, C. R.
- Affiliations
- Vanderbilt University Medical Center (US)
- American University of Beirut (LB)
- Corresponding author
- Flynn, Charles R.
- Venue
- Molecular Aspects of Medicine
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 56
- Pages
- 75-89
- ISSN
- 0098-2997 (ISSN-L)
- PMC
- PMC5603298
- OpenAlex
- W2607504605
- Cited by
- 148
- References
- 255
- Citations by year
- 2026: 12 · 2025: 16 · 2024: 19 · 2023: 17 · 2022: 17 · 2021: 15 · 2020: 19 · 2019: 12 · 2018: 10 · 2017: 11
- FWCI
- 3.01
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Molecular Aspects of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK091748, R01DK070860, R01DK105847, F32DK103474)
- Topics
- Health Sciences › Medicine › Surgery › Bariatric Surgery and Outcomes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- bile acids, bariatric surgery, Roux-en-Y gastric bypass, sleeve gastrectomy, morbid obesity, type 2 diabetes, enterohepatic circulation, gut microbiota, insulin sensitivity, glucose homeostasis, lipid homeostasis, energy expenditure, farnesoid X receptor, TGR5, bile acid receptors, rodent models
- MeSH terms
- Gastrointestinal Microbiome, Receptor, Farnesoid X-Activated, Animals, Bile Acids and Salts, Diabetes Mellitus, Type 2, Enterohepatic Circulation, Gastrectomy, Gene Expression Regulation, Glucose, Homeostasis, Humans, Insulin Resistance, Obesity, Morbid, Rodentia, Gastric Bypass, Signal Transduction, Receptors, Cytoplasmic and Nuclear, Receptors, G-Protein-Coupled
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