GPCR-Mediated Signaling of Metabolites
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
Standard
GPCR-Mediated Signaling of Metabolites. / Husted, Anna Sofie; Trauelsen, Mette; Rudenko, Olga; Hjorth, Siv A; Schwartz, Thue W.
I: Cell Metabolism, Bind 25, Nr. 4, 04.04.2017, s. 777-796.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - GPCR-Mediated Signaling of Metabolites
AU - Husted, Anna Sofie
AU - Trauelsen, Mette
AU - Rudenko, Olga
AU - Hjorth, Siv A
AU - Schwartz, Thue W
N1 - Copyright © 2017 Elsevier Inc. All rights reserved.
PY - 2017/4/4
Y1 - 2017/4/4
N2 - In addition to their bioenergetic intracellular function, several classical metabolites act as extracellular signaling molecules activating cell-surface G-protein-coupled receptors (GPCRs), similar to hormones and neurotransmitters. "Signaling metabolites" generated from nutrients or by gut microbiota target primarily enteroendocrine, neuronal, and immune cells in the lamina propria of the gut mucosa and the liver and, through these tissues, the rest of the body. In contrast, metabolites from the intermediary metabolism act mainly as metabolic stress-induced autocrine and paracrine signals in adipose tissue, the liver, and the endocrine pancreas. Importantly, distinct metabolite GPCRs act as efficient pro- and anti-inflammatory regulators of key immune cells, and signaling metabolites may thus function as important drivers of the low-grade inflammation associated with insulin resistance and obesity. The concept of key metabolites as ligands for specific GPCRs has broadened our understanding of metabolic signaling significantly and provides a number of novel potential drug targets.
AB - In addition to their bioenergetic intracellular function, several classical metabolites act as extracellular signaling molecules activating cell-surface G-protein-coupled receptors (GPCRs), similar to hormones and neurotransmitters. "Signaling metabolites" generated from nutrients or by gut microbiota target primarily enteroendocrine, neuronal, and immune cells in the lamina propria of the gut mucosa and the liver and, through these tissues, the rest of the body. In contrast, metabolites from the intermediary metabolism act mainly as metabolic stress-induced autocrine and paracrine signals in adipose tissue, the liver, and the endocrine pancreas. Importantly, distinct metabolite GPCRs act as efficient pro- and anti-inflammatory regulators of key immune cells, and signaling metabolites may thus function as important drivers of the low-grade inflammation associated with insulin resistance and obesity. The concept of key metabolites as ligands for specific GPCRs has broadened our understanding of metabolic signaling significantly and provides a number of novel potential drug targets.
KW - Journal Article
KW - Review
U2 - 10.1016/j.cmet.2017.03.008
DO - 10.1016/j.cmet.2017.03.008
M3 - Review
C2 - 28380372
VL - 25
SP - 777
EP - 796
JO - Cell Metabolism
JF - Cell Metabolism
SN - 1550-4131
IS - 4
ER -
ID: 180733432