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10.3390/ijms19020575 http://scihub22266oqcxt.onion/10.3390/ijms19020575 C5855797!5855797 !29462993     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29462993 &cmd=llinks): Failed to open stream: HTTP request failed! 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The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome |pdf=|usr=}}{{29462993 }} gab.com Text The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=29462993 #FOAvip Insulin signaling, as mediated through the insulin receptor (IR), plays a critical role in metabolism. Aberrations in this signaling cascade lead to several pathologies, the majority of which are classified under the umbrella term "metabolic syndrome". Although many of these pathologies are associated with insulin resistance, the exact mechanisms are not well understood. One area of current interest is the possibility of G-protein-coupled receptors (GPCRs) influencing or regulating IR signaling. This concept is particularly significant, because GPCRs have been shown to participate in cross-talk with the IR. More importantly, GPCR signaling has also been shown to preferentially regulate specific downstream signaling targets through GPCR agonist bias. A novel study recently demonstrated that this GPCR-biased agonism influences the activity of the IR without the presence of insulin. Although GPCR-IR cross-talk has previously been established, the notion that GPCRs can regulate the activation of the IR is particularly significant in relation to metabolic syndrome and other pathologies that develop as a result of alterations in IR signaling. As such, we aim to provide an overview of the physiological and pathophysiological roles of the IR within metabolic syndrome and its related pathologies, including cardiovascular health, gut microflora composition, gastrointestinal tract functioning, polycystic ovarian syndrome, pancreatic cancer, and neurodegenerative disorders. Furthermore, we propose that the GPCR-biased agonism may perhaps mediate some of the downstream signaling effects that further exacerbate these diseases for which the mechanisms are currently not well understood. Twit Text FOAVip The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=29462993 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29462993 #FOAvip English Wikipedia <ref>{{Cite pmid|29462993 }}</ref> The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between the Insulin Receptor and the Metabolic Syndrome #MMPMID29462993 Liauchonak I ; Dawoud F ; Riat Y ; Qorri B ; Sambi M ; Jain J ; Kalaydina RV ; Mendonza N ; Bajwa K ; Szewczuk MR Int J Mol Sci 2018[Feb]; 19 (2 ): ä PMID29462993 show ga Insulin signaling, as mediated through the insulin receptor (IR), plays a critical role in metabolism. Aberrations in this signaling cascade lead to several pathologies, the majority of which are classified under the umbrella term "metabolic syndrome". Although many of these pathologies are associated with insulin resistance, the exact mechanisms are not well understood. One area of current interest is the possibility of G-protein-coupled receptors (GPCRs) influencing or regulating IR signaling. This concept is particularly significant, because GPCRs have been shown to participate in cross-talk with the IR. More importantly, GPCR signaling has also been shown to preferentially regulate specific downstream signaling targets through GPCR agonist bias. A novel study recently demonstrated that this GPCR-biased agonism influences the activity of the IR without the presence of insulin. Although GPCR-IR cross-talk has previously been established, the notion that GPCRs can regulate the activation of the IR is particularly significant in relation to metabolic syndrome and other pathologies that develop as a result of alterations in IR signaling. As such, we aim to provide an overview of the physiological and pathophysiological roles of the IR within metabolic syndrome and its related pathologies, including cardiovascular health, gut microflora composition, gastrointestinal tract functioning, polycystic ovarian syndrome, pancreatic cancer, and neurodegenerative disorders. Furthermore, we propose that the GPCR-biased agonism may perhaps mediate some of the downstream signaling effects that further exacerbate these diseases for which the mechanisms are currently not well understood. |Cardiovascular Diseases/genetics/pathology [MESH] |Gastrointestinal Microbiome/genetics [MESH] |Humans [MESH] |Insulin/*genetics/metabolism [MESH] |Metabolic Syndrome/*genetics/pathology [MESH] |Pancreatic Neoplasms/genetics/pathology [MESH] |Receptor Cross-Talk [MESH] |Receptor, Insulin/agonists/*genetics [MESH] |Receptors, G-Protein-Coupled/agonists/*genetics [MESH]The Biased G-Protein-Coupled Receptor Agonism Bridges the Gap between (epmc).pdf DeepDyve Pubget Overpricing