The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome.

作者: Iryna Liauchonak , Fady Dawoud , Yatin Riat , Bessi Qorri , Manpreet Sambi

DOI: 10.3390/IJMS19020575

关键词: InsulinReceptorNeuroscienceG protein-coupled receptorInsulin receptorSignal transductionBiologyReceptor Cross-TalkMetabolic syndromeInsulin resistance

摘要: Insulin signaling, as mediated through the insulin receptor (IR), plays a critical role in metabolism. Aberrations this signaling cascade lead to several pathologies, majority of which are classified under umbrella term "metabolic syndrome". Although many these pathologies associated with resistance, exact mechanisms not well understood. One area current interest is possibility G-protein-coupled receptors (GPCRs) influencing or regulating IR signaling. This concept particularly significant, because GPCRs have been shown participate cross-talk IR. More importantly, GPCR has also preferentially regulate specific downstream targets agonist bias. A novel study recently demonstrated that GPCR-biased agonism influences activity without presence insulin. GPCR-IR previously established, notion can activation significant relation metabolic syndrome and other develop result alterations As such, we aim provide an overview physiological pathophysiological roles within its related including cardiovascular health, gut microflora composition, gastrointestinal tract functioning, polycystic ovarian syndrome, pancreatic cancer, neurodegenerative disorders. Furthermore, propose may perhaps mediate some effects further exacerbate diseases for currently

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