ArticleJournal of lipid research2017
Regulation of lipid metabolism by obeticholic acid in hyperlipidemic hamsters.
Article in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Comparative study of obeticholic acid and rosuvastatin in high-fat/fructose diet-induced metabolic dysfunction: role of AMPK, PPAR-γ, SREBP-1c, and STAT3 pathways.Journal of molecular histology · 2026Article
- Effects of Guanxinning tablet on the gut microbiota and bile acid metabolism in mice with hyperlipidemia.Frontiers in pharmacology · 2026Article
- Humanized mouse liver reveals endothelial control of essential hepatic metabolic functions.Cell · 2023Article
- Structure Optimization of 12β-Pharmaceuticals (Basel, Switzerland) · 2023Article
- Aquaporin-8 ameliorates hepatic steatosis through farnesoid X receptor in obese mice.iScience · 2023Article
- Obeticholic Acid Induces Hepatoxicity Via FXR in the NAFLD Mice.Frontiers in pharmacology · 2022Article
- Modulation of Bile Acid Metabolism to Improve Plasma Lipid and Lipoprotein Profiles.Journal of clinical medicine · 2021Review
- Euphornin L promotes lipid clearance by dual regulation of LDLR and PCSK9.Experimental and therapeutic medicine · 2021Article
- FXR activation promotes intestinal cholesterol excretion and attenuates hyperlipidemia in SR-B1-deficient mice fed a high-fat and high-cholesterol diet.Physiological reports · 2020Article
- Obeticholic acid ameliorates dyslipidemia but not glucose tolerance in mouse model of gestational diabetes.American journal of physiology. Endocrinology and metabolism · 2019Article
- Activation of FXR by obeticholic acid induces hepatic gene expression of SR-BI through a novel mechanism of transcriptional synergy with the nuclear receptor LXR.International journal of molecular medicine · 2019Article
- Liver-specific knockdown of long-chain acyl-CoA synthetase 4 reveals its key role in VLDL-TG metabolism and phospholipid synthesis in mice fed a high-fat diet.American journal of physiology. Endocrinology and metabolism · 2019Article
- Bile acids promote gastric intestinal metaplasia by upregulating CDX2 and MUC2 expression via the FXR/NF-κB signalling pathway.International journal of oncology · 2019Article
- Farnesoid X Receptor Activation by Obeticholic Acid Elevates Liver Low-Density Lipoprotein Receptor Expression by mRNA Stabilization and Reduces Plasma Low-Density Lipoprotein Cholesterol in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- FXR activation by obeticholic acid or nonsteroidal agonists induces a human-like lipoprotein cholesterol change in mice with humanized chimeric liver.Journal of lipid research · 2018Article
- Bile acids at the cross-roads of gut microbiome-host cardiometabolic interactions.Diabetology & metabolic syndrome · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The farnesoid X receptor (FXR) plays critical roles in plasma cholesterol metabolism, in particular HDL-cholesterol (HDL-C) homeostasis. Obeticholic acid (OCA) is a FXR agonist being developed for treating various chronic liver diseases. Previous studies reported inconsistent effects of OCA on regulating plasma cholesterol levels in different animal models and in different patient populations. The mechanisms underlying its divergent effects have not yet been thoroughly investigated. The scavenger receptor class B type I (SR-BI) is a FXR-modulated gene and the major receptor for HDL-C. We investigated the effects of OCA on hepatic SR-BI expression and correlated such effects with plasma HDL-C levels and hepatic cholesterol efflux in hyperlipidemic hamsters. We demonstrated that OCA induced a time-dependent reduction in serum HDL-C levels after 14 days of treatment, which was accompanied by a significant reduction of liver cholesterol content and increases in fecal cholesterol in OCA-treated hamsters. Importantly, hepatic SR-BI mRNA and protein levels in hamsters were increased to 1.9- and 1.8-fold of control by OCA treatment. Further investigations in normolipidemic hamsters did not reveal OCA-induced changes in serum HDL-C levels or hepatic SR-BI expression. We conclude that OCA reduces plasma HDL-C levels and promotes transhepatic cholesterol efflux in hyperlipidemic hamsters via a mechanism involving upregulation of hepatic SR-BI.
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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 OpenQuestion graph.