Metabolite G-Protein Coupled Receptors in Cardio-Metabolic Diseases

G protein-coupled receptors (GPCRs) have originally been described as a family of receptors activated by hormones, neurotransmitters, and other mediators. However, in recent years GPCRs have shown to bind endogenous metabolites, which serve functions other than as signaling mediators. These receptor...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2021-11, Vol.10 (12), p.3347
Main Authors: Strassheim, Derek, Sullivan, Timothy, Irwin, David C, Gerasimovskaya, Evgenia, Lahm, Tim, Klemm, Dwight J, Dempsey, Edward C, Stenmark, Kurt R, Karoor, Vijaya
Format: Article
Language:English
Subjects:
Animals
Bile acids
Body fat
cardiovascular
Cardiovascular diseases
Cardiovascular Diseases - metabolism
Diabetes mellitus
Disaccharides
Dyslipidemia
Fatty acids
G protein-coupled receptors
GPCR
Humans
inflammation
Insulin resistance
Intermediates
Ketones
Lactic acid
Ligands
Metabolic Diseases - metabolism
Metabolic disorders
metabolic syndrome
Metabolites
Metabolome
Models, Biological
Neurotransmitters
Obesity
Oxidation
Receptors, G-Protein-Coupled - metabolism
Review
Therapeutic targets
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Summary:G protein-coupled receptors (GPCRs) have originally been described as a family of receptors activated by hormones, neurotransmitters, and other mediators. However, in recent years GPCRs have shown to bind endogenous metabolites, which serve functions other than as signaling mediators. These receptors respond to fatty acids, mono- and disaccharides, amino acids, or various intermediates and products of metabolism, including ketone bodies, lactate, succinate, or bile acids. Given that many of these metabolic processes are dysregulated under pathological conditions, including diabetes, dyslipidemia, and obesity, receptors of endogenous metabolites have also been recognized as potential drug targets to prevent and/or treat metabolic and cardiovascular diseases. This review describes G protein-coupled receptors activated by endogenous metabolites and summarizes their physiological, pathophysiological, and potential pharmacological roles.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells10123347