Bile acids are nutrient signaling hormones
Open accessAbstract
Bile salts play crucial roles in allowing the gastrointestinal system to digest, transport and metabolize nutrients. They function as nutrient signaling hormones by activating specific nuclear receptors (FXR, PXR, Vitamin D) and G-protein coupled receptors [TGR5, sphingosine-1 phosphate receptor 2 (S1PR2), muscarinic receptors]. Bile acids and insulin appear to collaborate in regulating the metabolism of nutrients in the liver. They both activate the AKT and ERK1/2 signaling pathways. Bile acid induction of the FXR-α target gene, small heterodimer partner (SHP), is highly dependent on the activation PKCζ, a branch of the insulin signaling pathway. SHP is an important regulator of glucose and lipid metabolism in the liver. One might hypothesize that chronic low grade inflammation which is associated with insulin resistance, may inhibit bile acid signaling and disrupt lipid metabolism. The disruption of these signaling pathways may increase the risk of fatty liver and non-alcoholic fatty liver disease (NAFLD). Finally, conjugated bile acids appear to promote cholangiocarcinoma growth via the activation of S1PR2.
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Some secondary bile acids impact host physiology through interaction with host nuclear receptors including FXR, LXR, PXR, and specific G-protein coupled receptors like TGR5.
“Following systemic adsorption, some secondary BAs in turn impact host physiology though interaction with a variety of host nuclear receptors including FXR, liver X receptor (LXR), pregnane X receptor (PXR), and specific G-protein coupled receptors like TGR5 (Figure 1)40–44.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [42]
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- Authors
- Zhou, H., & Hylemon, P. B.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Zhou, Huiping
- Hylemon, Phillip B.
- Venue
- Steroids
- Publisher
- Elsevier BV
- Published
- 2014-08
- Volume
- 86
- Pages
- 62-68
- ISSN
- 0039-128X (ISSN-L)
- PMC
- PMC4073476
- OpenAlex
- W2075781716
- Cited by
- 285
- References
- 73
- Citations by year
- 2026: 14 · 2025: 20 · 2024: 19 · 2023: 30 · 2022: 29 · 2021: 29 · 2020: 24 · 2019: 23 · 2018: 30 · 2017: 25 · 2016: 26 · 2015: 11 · 2014: 5
- FWCI
- 2.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Steroids (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX001390)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK057543)
- Topics
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- bile acids, farnesoid X receptor, pregnane X receptor, vitamin D receptor, TGR5, S1PR2, muscarinic receptors, insulin signaling, Akt signaling, ERK signaling, protein kinase C, small heterodimer partner, hepatic metabolism, insulin resistance, chronic inflammation, non-alcoholic fatty liver disease, cholangiocarcinoma, bile acid conjugates
- MeSH terms
- Bile Acids and Salts, Food, Glucose, Humans, Metabolic Diseases, Signal Transduction, Receptors, Cytoplasmic and Nuclear, Receptors, G-Protein-Coupled, Lipid Metabolism
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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