ReviewComprehensive Physiology2013
Bile acid metabolism and signaling.
Review in Comprehensive Physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07120828 (The Role of CYP8B1 Polymorphisms in Modulating the Biochemical Pathways Affected by SGLT2 Inhibitors in T2DM and Obesity), which is not on this map. Cited by 824 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
The Role of CYP8B1 Polymorphisms in Modulating the Biochemical Pathways Affected by SGLT2 Inhibitors in T2DM and Obesity
Who cites it
824 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,388 citations in OpenAlex.
- Pooled it
- Pharmacological Mechanisms of Bile Acids Targeting the Farnesoid X Receptor.International journal of molecular sciences · 2024Pooled it
- Gut microbial bile and amino acid metabolism associate with peanut oral immunotherapy failure.Nature communications · 2025Trial
- Article
- How lipid ingestion is sensed: the mechanisms underlying intestinal hormone secretion.Clinical science (London, England : 1979) · 2026Review
- Bile acid signaling in health and disease.Molecular biomedicine · 2026Review
- Fermented protein foods as modulators of the gut-muscle axis: mechanisms, evidence, and future directions.Communications biology · 2026Review
- Targeting the Gut Microbiome in Cardiovascular Disease: Current Therapeutic Strategies and Future Perspectives.Nutrients · 2026Review
- Bile Acid Metabolism as a Unifying Readout for Diet, Microbiome Function, and Gastrointestinal Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Fasting Serum Bile Acid Profiles in Dogs with Food-Responsive and Immunosuppressant-Responsive Chronic Inflammatory Enteropathy: An Exploratory LC-MS/MS Study.Animals : an open access journal from MDPI · 2026Article
- From metabolites to membrane vesicles: Unifying gut microbial signals in obesity, t2dm, and MASLD.World journal of microbiology & biotechnology · 2026Review
- Dysregulated bile acid metabolism impairs intestinal barrier integrity via defective GPBAR1 signaling in low-birth-weight suckling piglet.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Pulsatile FXR activation: Timing bile acid-targeted therapy to physiology.Acta pharmacologica Sinica · 2026Article
- Dietary bile acids supplementation reduces eggshell translucency and improves eggshell quality in late-phase laying hens.Poultry science · 2026Article
- hypeR-GEM: connecting metabolite signatures to enzyme-coding genes via genome-scale metabolic models.Bioinformatics (Oxford, England) · 2026Article
- Gut Microbiota in Metabolic Syndrome: Differences in Microbial Signatures and Clinical Profiles.Medicina (Kaunas, Lithuania) · 2026Review
- Hypercholesterolemia induced by hypothyroidism is ameliorated by taurine supplementation through the hepatic AMPK/ACC pathway.Archives of endocrinology and metabolism · 2026Article
- Ordering molecular diversity in untargeted metabolomics via molecular community networking.Cell reports methods · 2026Article
- Cell line identity rather than medium composition determines transcriptomic profiles of HepaRG and HuH7 cells cultured in chemically defined or serum-based media: comparison with primary human hepatocytes.Archives of toxicology · 2026Article
- Gut Microbiota and Atherosclerotic Plaque Instability: Cellular and Molecular Mechanisms.International journal of molecular sciences · 2026Review
764 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Bile acids are important physiological agents for intestinal nutrient absorption and biliary secretion of lipids, toxic metabolites, and xenobiotics. Bile acids also are signaling molecules and metabolic regulators that activate nuclear receptors and G protein-coupled receptor (GPCR) signaling to regulate hepatic lipid, glucose, and energy homeostasis and maintain metabolic homeostasis. Conversion of cholesterol to bile acids is critical for maintaining cholesterol homeostasis and preventing accumulation of cholesterol, triglycerides, and toxic metabolites, and injury in the liver and other organs. Enterohepatic circulation of bile acids from the liver to intestine and back to the liver plays a central role in nutrient absorption and distribution, and metabolic regulation and homeostasis. This physiological process is regulated by a complex membrane transport system in the liver and intestine regulated by nuclear receptors. Toxic bile acids may cause inflammation, apoptosis, and cell death. On the other hand, bile acid-activated nuclear and GPCR signaling protects against inflammation in liver, intestine, and macrophages. Disorders in bile acid metabolism cause cholestatic liver diseases, dyslipidemia, fatty liver diseases, cardiovascular diseases, and diabetes. Bile acids, bile acid derivatives, and bile acid sequestrants are therapeutic agents for treating chronic liver diseases, obesity, and diabetes in humans.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.