Cited by 248Drug Transport and Resistance MechanismsCholesterol and Lipid MetabolismGut microbiota and health

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The Role of Bile Acids in Glucose Metabolism and Their Relation with Diabetes

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Alberto González-Regueiro, José, Moreno-Castañeda, Lidia, Uribe, Misael, Carlos Chávez-Tapia, Norberto·2017·Annals of Hepatology

DOI 10.5604/01.3001.0010.5494

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Abstract

Bile acids (BAs), the end products of cholesterol catabolism, are essential for the absorption of lipids and fat-soluble vitamins; but they have also emerged as novel signaling molecules that act as metabolic regulators. It has been well described that the enterohe-patic circulation, a nuclear (FXR) and a cytoplasmic (TGR5/M-BAR) receptor aid in controlling hepatic bile acid synthesis. Modulating bile acid synthesis greatly impacts in metabolism, because these receptors also are implicated in glucose, lipid, and energy expenditure. Recent studies had revealed the way these receptors participate in regulating gluconeogenesis, peripheral insulin sensitivity, glycogen synthesis, glucagon like peptide 1 (GLP-1) and insulin secretion. Nowadays, it is demonstrated that enhancing bile acid signaling in the intestine contributes to the metabolic benefits of bile acid sequestrants and bariatric surgery on glucose homeos-tasis. This paper discusses the role of bile acid as regulators of glucose metabolism and their potential as therapeutic targets for diabetes.

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Figure 1 Enterohepatic negative feedback mechanisms of bile acid synthesis. BAs are synthetized from cholesterol molecules in the hepatocyte and then are stored in the gallbladder. After meal ingestion, they are released into the intestine where they activate FXR and TGR5. BAs are reabsorbed through the ASBT, activating FXR at the enterocyte, which produces a negative feedback mechanism in the synthesis of bile acids. FXR activation also stimulates FGF-19, which concomitantly participates in the negative feedback mechanism at the hepatocyte. The activation of TGR5 increases secretion of GLP-1. CYP7A1: cholesterol-7 A -hydroxylase. BA: bile acid. SHP: small heterodimer partner. FXR: farnesoid X receptor. FGFR4: fibroblast growth factor receptor-4. FGF19: fibroblast growth factor-19. ASBT: apical sodium-dependent bile salt transporter. TGR5: G protein-coupled receptor TGR5. GLP1: glucagon like peptide 1. Adapted from Sonne, et al. 2014. 49CC-BY-NC-ND · From the PDF

Figure 2 Bile acid mediated regulation of glucose metabolism. After meal ingestion, BAs are released into the intestine where they activate FXR and TGR5. FXR activation stimulates FGF19, which participates in glycogen synthesis and gluconeogenesis. TGR5 activation increases levels of GLP-1, promoting insulin secretion and decreased serum glucose levels. BAs that are reabsorbed through the enterohepatic circulation activate FXR in the liver, which also participates in gluconeogenesis and glycolysis. BA: Bile acid. FXR: farnesoid X receptor. TGR5: G protein-coupled receptor TGR5. FGF19: fibroblast growth factor-19. GLP1: glucagon like peptide 1. Adapted from Sonne, et al. 2014. 49CC-BY-NC-ND · From the PDF

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Authors: Alberto González-Regueiro, J., Moreno-Castañeda, L., Uribe, M., & Carlos Chávez-Tapia, N.
Affiliations: Hospital Médica Sur (MX)
ORCID: Uribe, Misael
Venue: Annals of Hepatology
Publisher: Elsevier BV
Published: 2017-11
Volume: 16
Issue: Suppl. 1: s3-105.
Pages: S15-S20
ISSN: 1665-2681 (ISSN-L)
DOI: 10.5604/01.3001.0010.5494
OpenAlex: W3194266802
Cited by: 247
References: 49
Citations by year: 2026: 25 · 2025: 26 · 2024: 43 · 2023: 34 · 2022: 34 · 2021: 38 · 2020: 20 · 2019: 12 · 2018: 15
FWCI: 5.70
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor, 586 d)
Locations: Annals of Hepatology (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Australian Government
Topics: Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
Keywords: bile acids, glucose metabolism, diabetes mellitus, enterohepatic circulation, farnesoid X receptor, TGR5, bile acid synthesis, gluconeogenesis, insulin sensitivity, glycogen synthesis, glucagon-like peptide-1, insulin secretion, bile acid sequestrants, bariatric surgery, glucose homeostasis, therapeutic target
MeSH terms: Gastrointestinal Microbiome, Animals, Bacteria, Bile Acids and Salts, Energy Metabolism, Humans, Intestines, Obesity, Signal Transduction, Host-Pathogen Interactions, Dysbiosis

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The Role of Bile Acids in Glucose Metabolism and Their Relation with Diabetes

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