Special Issue "100th Anniversary of Insulin: Insulin Receptor Signaling in Health and Disease"
Deadline for manuscript submissions: 31 August 2022 | Viewed by 3650
Interests: immunology; COVID-19 and ACE2 receptor; cancer; inflammation; TLR receptor; Trk receptor; GPCR signaling; insulin receptor; glycosylation; NEU1 sialidase
Several signaling molecules have been identified as critical players in the regulation of insulin-induced IR activation. G protein-coupled receptors (GPCR) have recently been implicated in intracellular crosstalk pathways with IR. The integration of GPCR and receptor tyrosine kinase (RTK) signaling, including IR upon ligand stimulation, is eloquently reviewed. Other reports have also shown that IR can interact with Gαi subunits upon receptor activation. An upregulation of IR expression and its activation is significantly associated with higher downstream G protein signaling cascades. G protein stoichiometry can dictate biased agonism through distinct receptor-G protein partitioning. The expression levels of Gα subunits influence the biased profiling of β-agonists and antagonists in that they determine both their activity and efficacy by affecting different membrane distribution of receptor-G protein populations. In the naïve state, the level of Gα expression influences the partitioning of not only Gα but also the co-expressed receptor in different membrane domains. This intriguing concept could explain where GPCR activation mutations correlate with increased downstream IR signaling in the complete absence of insulin. Can this G-protein signaling platform preassociate with insulin receptors with non-nutrition artificial sweetners, gut microbiome metabolites, μ-opioid and cannabinoid CB GPCRs? The gaps in our knowledge regarding how these metabolite consumptions are implicated in host metabolism via GPCR receptors reinforce the importance of research needed to understand the mechanistic action of these drugs on the body as promising metabolic candidates.
Collectively, these findings uncover a unique mode of control for IR activation and present an innovative approach to targeting insulin signaling via GPCR complexes. The key players potentiating receptor GPCR biased signaling of IRβ receptors can advance our understanding of the current dogma(s) governing crosstalks between GPCR biased metabolites and cellular responses contributing to diabetes. This research has the potential to uncover (a) novel mechanism(s) of metabolite-induced metabolic changes, epigenetic reprogramming, insulin resistance and diabetes.
Original manuscripts and reviews dealing with any aspect of insulin receptor and related pathophysiology are welcome.
Dr. Myron R. Szewczuk
Dr. Fiona Haxho
Manuscript Submission Information
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- insulin receptor
- IR signaling
- GPCR signaling
- insulin resistance
- non-nutritional artificial sweeteners
- gut microbiome metabolites
- metabolic syndrome
- angiotensin I
- angiotensin II
- neu1 sialidase
- NMBR receptors
- G protein-coupled receptor
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: To be determined
Authors: Jyoti C Patel; Kenneth D Carr; Margaret Rice
Affiliation: NYU Grossman School of Medicine, USA