NDLI: Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Feingold, Kenneth R. Moser, Arthur Shigenaga, Judy K. Grunfeld, Carl
Description	Author Affiliation: Feingold KR ( Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, San Francisco, CA 94121.); Moser A ( Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, San Francisco, CA 94121.); Shigenaga JK ( Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, San Francisco, CA 94121.); Grunfeld C ( Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, San Francisco, CA 94121.)
Abstract	Many of the beneficial and adverse effects of niacin are mediated via a G protein receptor, G protein-coupled receptor 109A/hydroxycarboxylic acid 2 receptor (GPR109A/HCA2), which is highly expressed in adipose tissue and macrophages. Here we demonstrate that immune activation increases GPR109A/HCA2 expression. Lipopolysaccharide (LPS), TNF, and interleukin (IL) 1 increase GPR109A/HCA2 expression 3- to 5-fold in adipose tissue. LPS also increased GPR109A/HCA2 mRNA levels 5.6-fold in spleen, a tissue rich in macrophages. In peritoneal macrophages and RAW cells, LPS increased GPR109A/HCA2 mRNA levels 20- to 80-fold. Zymosan, lipoteichoic acid, and polyinosine-polycytidylic acid, other Toll-like receptor activators, and TNF and IL-1 also increased GPR109A/HCA2 in macrophages. Inhibition of the myeloid differentiation factor 88 or TIR-domain-containing adaptor protein inducing IFNß pathways both resulted in partial inhibition of LPS stimulation of GPR109A/HCA2, suggesting that LPS signals an increase in GPR109A/HCA2 expression by both pathways. Additionally, inhibition of NF-κB reduced the ability of LPS to increase GPR109A/HCA2 expression by â¼50% suggesting that both NF-κB and non-NF-κB pathways mediate the LPS effect. Finally, preventing the LPS-induced increase in GPR109A/HCA2 resulted in an increase in TG accumulation and the expression of enzymes that catalyze TG synthesis. These studies demonstrate that inflammation stimulates GPR109A/HCA2 and there are multiple intracellular signaling pathways that mediate this effect. The increase in GPR109A/HCA2 that accompanies macrophage activation inhibits the TG accumulation stimulated by macrophage activation.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M050955
Journal	The Journal of Lipid Research
Issue Number	12
Volume Number	55
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2014-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Disease Models, Animal Intra-abdominal Fat Metabolism Macrophage Activation Macrophages, Peritoneal Receptors, G-protein-coupled Receptors, Nicotinic Signal Transduction Up-regulation 3t3-l1 Cells Animals Cell Line, Transformed Cells, Cultured Gram-negative Bacterial Infections Immunology Pathology Gram-positive Bacterial Infections Lipid Metabolism Mice Mice, Inbred C57bl Mycoses Rna Interference Antagonists & Inhibitors Genetics Virus Diseases Comparative Study Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages

Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages

Granulocyte/Macrophage Colony-stimulating Factor-dependent Dendritic Cells Restrain Lean Adipose Tissue Expansion.

Lipoprotein lipase suppression in 3T3-L1 cells by an endotoxin-induced mediator from exudate cells.

Bacterial lipopolysaccharide stimulates protein tyrosine phosphorylation in macrophages.

Increased GIP signaling induces adipose inflammation via a HIF-1 -dependent pathway and impairs insulin sensitivity in mice.

Involvement of mast cells in adipose tissue fibrosis.

A role for connexin43 in macrophage phagocytosis and host survival after bacterial peritoneal infection.

Role of adiponectin in adipose tissue wound healing.

Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages.

Similar Documents

Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages

Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages

Granulocyte/Macrophage Colony-stimulating Factor-dependent Dendritic Cells Restrain Lean Adipose Tissue Expansion.

Lipoprotein lipase suppression in 3T3-L1 cells by an endotoxin-induced mediator from exudate cells.

Bacterial lipopolysaccharide stimulates protein tyrosine phosphorylation in macrophages.

Increased GIP signaling induces adipose inflammation via a HIF-1 -dependent pathway and impairs insulin sensitivity in mice.

Involvement of mast cells in adipose tissue fibrosis.

A role for connexin43 in macrophage phagocytosis and host survival after bacterial peritoneal infection.

Role of adiponectin in adipose tissue wound healing.

Inflammation stimulates niacin receptor (GPR109A/HCA2) expression in adipose tissue and macrophages.