Evidence of functional bile acid signaling pathways in adipocytes.


Journal

Molecular and cellular endocrinology
ISSN: 1872-8057
Titre abrégé: Mol Cell Endocrinol
Pays: Ireland
ID NLM: 7500844

Informations de publication

Date de publication:
01 03 2019
Historique:
received: 10 07 2018
revised: 29 11 2018
accepted: 10 12 2018
pubmed: 14 12 2018
medline: 27 11 2019
entrez: 14 12 2018
Statut: ppublish

Résumé

Bile acids (BA) are increasingly recognized as pleiotropic and hormone-like signaling molecules with metabolic and endocrine functions. However, the role of BA in white adipocyte physiology remains somewhat obscure. It was the aim to investigate the BA receptors (FXR, TGR5) and FGFR1 (Fibroblast growth factor receptor 1) as well as Bsep (bile salt export pump) in white adipocytes and in murine and human adipose tissue (AT) and to investigate effects of different BA species in adipocyte physiology. Receptor mRNA expression was quantified by real-time PCR in mice, humans and during 3T3-L1 pre-adipocyte differentiation. Adipokines were measured by ELISA upon stimulation by several BA. Effects of BA on TNF- and LPS-induced MCP-1 secretion and lipolysis were analyzed. TNF-induced lipolysis was investigated by glycerol assay. The present data provide for the first time a detailed expression profile of FXR, TGR5, FGFR1, and Bsep during adipocyte differentiation and in murine and human AT. FGFR1 expression is upregulated in adipose tissue of LPS-injected animals. Several BA regulate secretion of adipokines such as adiponectin and resistin differentially. Importantly, TNF- and LPS-induced MCP-1 release from adipocytes as well as TNF-induced lipolysis can be antagonized by cholic acid (CA) and deoxycholic acid (DCA). The present data provide evidence of functional BA signaling pathways in adipocytes and argue for certain MCP-1 related anti-inflammatory effects of BA in TNF- and LPS-induced inflammation, whereas pro-inflammatory resistin is induced by CA and glycocholic acid (GCA). Systemic bile acids might represent a hormonal network regulating white adipocyte physiology including lipolysis.

Sections du résumé

BACKGROUND AND AIM
Bile acids (BA) are increasingly recognized as pleiotropic and hormone-like signaling molecules with metabolic and endocrine functions. However, the role of BA in white adipocyte physiology remains somewhat obscure. It was the aim to investigate the BA receptors (FXR, TGR5) and FGFR1 (Fibroblast growth factor receptor 1) as well as Bsep (bile salt export pump) in white adipocytes and in murine and human adipose tissue (AT) and to investigate effects of different BA species in adipocyte physiology.
PATIENTS, MATERIAL AND METHODS
Receptor mRNA expression was quantified by real-time PCR in mice, humans and during 3T3-L1 pre-adipocyte differentiation. Adipokines were measured by ELISA upon stimulation by several BA. Effects of BA on TNF- and LPS-induced MCP-1 secretion and lipolysis were analyzed. TNF-induced lipolysis was investigated by glycerol assay.
RESULTS
The present data provide for the first time a detailed expression profile of FXR, TGR5, FGFR1, and Bsep during adipocyte differentiation and in murine and human AT. FGFR1 expression is upregulated in adipose tissue of LPS-injected animals. Several BA regulate secretion of adipokines such as adiponectin and resistin differentially. Importantly, TNF- and LPS-induced MCP-1 release from adipocytes as well as TNF-induced lipolysis can be antagonized by cholic acid (CA) and deoxycholic acid (DCA).
CONCLUSIONS
The present data provide evidence of functional BA signaling pathways in adipocytes and argue for certain MCP-1 related anti-inflammatory effects of BA in TNF- and LPS-induced inflammation, whereas pro-inflammatory resistin is induced by CA and glycocholic acid (GCA). Systemic bile acids might represent a hormonal network regulating white adipocyte physiology including lipolysis.

Identifiants

pubmed: 30543876
pii: S0303-7207(18)30359-9
doi: 10.1016/j.mce.2018.12.006
pii:
doi:

Substances chimiques

ATP Binding Cassette Transporter, Subfamily B, Member 11 0
Adipokines 0
Bile Acids and Salts 0
Lipopolysaccharides 0
Receptors, Cytoplasmic and Nuclear 0
Receptors, G-Protein-Coupled 0
farnesoid X-activated receptor 0C5V0MRU6P
Receptor, Fibroblast Growth Factor, Type 1 EC 2.7.10.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-10

Informations de copyright

Copyright © 2018. Published by Elsevier B.V.

Auteurs

Andreas Schmid (A)

Department of Internal Medicine III, Giessen University Hospital, Germany. Electronic address: andreas.schmid@innere.med.uni-giessen.de.

Jutta Schlegel (J)

Department of Internal Medicine III, Giessen University Hospital, Germany.

Miriam Thomalla (M)

Department of Internal Medicine III, Giessen University Hospital, Germany.

Thomas Karrasch (T)

Department of Internal Medicine III, Giessen University Hospital, Germany.

Andreas Schäffler (A)

Department of Internal Medicine III, Giessen University Hospital, Germany.

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Classifications MeSH