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http://purl.uniprot.org/citations/38206814http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/38206814http://www.w3.org/2000/01/rdf-schema#comment"Mitochondrial Ca2+ ([Ca2+]m) homeostasis is critical for β-cell function and becomes disrupted during the pathogenesis of diabetes. [Ca2+]m uptake is dependent on elevations in cytoplasmic Ca2+ ([Ca2+]c) and endoplasmic reticulum Ca2+ ([Ca2+]ER) release, both of which are regulated by the two-pore domain K+ channel TALK-1. Here, utilizing a novel β-cell TALK-1-knockout (β-TALK-1-KO) mouse model, we found that TALK-1 limited β-cell [Ca2+]m accumulation and ATP production. However, following exposure to a high-fat diet (HFD), ATP-linked respiration, glucose-stimulated oxygen consumption rate, and glucose-stimulated insulin secretion (GSIS) were increased in control but not TALK1-KO mice. Although β-TALK-1-KO animals showed similar GSIS before and after HFD treatment, these mice were protected from HFD-induced glucose intolerance. Collectively, these data identify that TALK-1 channel control of β-cell function reduces [Ca2+]m and suggest that metabolic remodeling in diabetes drives dysglycemia."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.org/dc/terms/identifier"doi:10.1016/j.celrep.2024.113673"xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Dobson J.R."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Jacobson D.A."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Dadi P.K."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Vierra N.C."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Dickerson M.T."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Zaborska K.E."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Graff S.M."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Nakhe A.Y."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Butterworth R.B."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/author"Ibsen C.E."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/date"2024"xsd:gYear
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/name"Cell Rep"xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/pages"113673"xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/title"TALK-1-mediated alterations of beta-cell mitochondrial function and insulin secretion impair glucose homeostasis on a diabetogenic diet."xsd:string
http://purl.uniprot.org/citations/38206814http://purl.uniprot.org/core/volume"43"xsd:string
http://purl.uniprot.org/citations/38206814http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/38206814
http://purl.uniprot.org/citations/38206814http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/38206814
http://purl.uniprot.org/uniprot/#_G5E845-mappedCitation-38206814http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38206814
http://purl.uniprot.org/uniprot/G5E845http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/38206814