ArticleBiochemical pharmacology2010
Modulation of HDL metabolism by the niacin receptor GPR109A in mouse hepatocytes.
Article in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 51 citations in OpenAlex.
- Bile Canalicular Bitter Taste Receptors Inhibit β-Adrenergic Receptor-Induced Lipolysis in Steatotic Hepatocytes.International journal of molecular sciences · 2026Article
- GPCRs involved in metabolic diseases: pharmacotherapeutic development updates.Acta pharmacologica Sinica · 2024Review
- Balancing NADCellular and molecular life sciences : CMLS · 2022Review
- The Role of GPR109a Signaling in Niacin Induced Effects on Fed and Fasted Hepatic Metabolism.International journal of molecular sciences · 2021Article
- G protein-coupled receptors as potential targets for nonalcoholic fatty liver disease treatment.World journal of gastroenterology · 2021Review
- GPR109A mediates the effects of hippuric acid on regulating osteoclastogenesis and bone resorption in mice.Communications biology · 2021Article
- Metabolic Functions of G Protein-Coupled Receptors in Hepatocytes-Potential Applications for Diabetes and NAFLD.Biomolecules · 2020Review
- GPR109A activation and aging liver.Aging · 2019Article
- Niacin improves maturation and cryo-tolerance of bovine in vitro matured oocytes: An experimental study.International journal of reproductive biomedicine · 2019Article
- Review
- Implications of altered NAD metabolism in metabolic disorders.Journal of biomedical science · 2019Review
- Butyrate, a metabolite of intestinal bacteria, enhances sleep.Scientific reports · 2019Article
- Dimethyl fumarate mediates Nrf2-dependent mitochondrial biogenesis in mice and humans.Human molecular genetics · 2017Article
- Dietary Niacin Supplementation Suppressed Hepatic Lipid Accumulation in Rabbits.Asian-Australasian journal of animal sciences · 2016Article
- NAD(+) Metabolism and the Control of Energy Homeostasis: A Balancing Act between Mitochondria and the Nucleus.Cell metabolism · 2015Review
- Gut microbiota-derived short-chain Fatty acids, T cells, and inflammation.Immune network · 2014Review
- Screening of Different Organs of Rats for HCA2 Receptor mRNA.International journal of molecular and cellular medicine · 2014Article
- L-2-oxothiazolidine-4-carboxylic acid attenuates oxidative stress and inflammation in retinal pigment epithelium.Molecular vision · 2014Article
- Nicotinic acid inhibits hepatic APOA gene expression: studies in humans and in transgenic mice.Journal of lipid research · 2012Article
- G protein-coupled receptors for energy metabolites as new therapeutic targets.Nature reviews. Drug discovery · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The niacin receptor GPR109A is a G(i)-protein-coupled receptor which mediates the effects of niacin on inhibiting intracellular triglyceride lipolysis in adipocytes. However, the role of GPR109A in mediating the effects of niacin on high density lipoprotein (HDL) metabolism is unclear. We found niacin has no effect on HDL-C in GPR109A knockout mice. Furthermore, niacin lowered intracellular cAMP in primary hepatocytes mediated by GPR109A. We used an adeno-associated viral (AAV) serotype 8 vector encoding GPR109A under the control of the hepatic-specific thyroxine-binding globulin promoter to specifically overexpress GPR109A in mouse liver. Plasma HDL-C, hepatic ABCA1 and the HDL cholesterol production rate were significantly reduced in mice overexpressing GPR109A. Overexpression of GPR109A reduced primary hepatocyte free cholesterol efflux to apoA-I; conversely, GPR109A deficient hepatocytes had increased ABCA1-mediated cholesterol efflux. These data support the concept that the HDL-C lowering effect of niacin in wild-type mice is mediated through stimulation of GPR109A in hepatocytes; such an effect then leads to reduced hepatocyte ABCA1 expression and activity, decreased cholesterol efflux to nascent apoA-I, and reduced HDL-C levels. These results indicate that niacin-mediated activation of GP109A in liver lowers ABCA1 expression leading to reduced hepatic cholesterol efflux to HDL.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.