FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1992295816> ?p ?o ?g. }

• W1992295816 endingPage "e15845" @default.
• W1992295816 startingPage "e15845" @default.
• W1992295816 abstract "Background Over-activity and elevated expression of glycogen synthase kinase-3 (GSK-3) has been implicated in the etiology of insulin resistance and Type 2 diabetes. Administration of specific GSK-3 inhibitors to diabetic or obese rodent models improves glycaemic control and insulin sensitivity. However, due to the indiscriminatory nature of these inhibitors, the relative contribution of the two isoforms of GSK-3 (GSK-3α and GSK-3β) is not known. Recently, we demonstrated that an out-bred strain of mice (ICR) lacking expression of GSK-3α in all tissues displayed improved insulin sensitivity and enhanced hepatic glucose metabolism. We also found that muscle (but not liver) inactivation of GSK-3β conferred insulin and glucose sensitization in an in-bred strain of mice (C57BL/6). Methodology/Principal Findings Here, we have employed tissue-specific deletion of GSK-3α, to examine the relative contribution of two insulin-sensitive tissues, muscle and liver, towards the insulin sensitization phenotype originally observed in the global GSK-3α KO animals. We found that mice in which GSK-3α has been inactivated in either skeletal-muscle or liver displayed no differences in glucose tolerance or insulin sensitivity compared to wild type littermates. Given the strain differences in our original analyses, we examined the insulin and glucose sensitivity of global GSK-3α KO animals bred onto a C57BL/6 background. These animals also revealed no significant differences in glucose metabolism/insulin sensitivity compared to their wild type littermates. Furthermore, deletion of hepatic GSK-3α on the out-bred, ICR background failed to reproduce the insulin sensitivity manifested by the global deletion of this isoform. Conclusions/Significance From these data we conclude that the improved insulin sensitivity and hepatic glucose homeostasis phenotype observed upon global inactivation of GSK-3α is strain-specific. We surmise that the insulin-sensitization observed in the out-bred strain of mice lacking GSK-3α is mediated by indirect means that do not require intrinsic function of GSK-3α in skeletal muscle and liver tissues." @default.
• W1992295816 created "2016-06-24" @default.
• W1992295816 creator A5033476856 @default.
• W1992295816 creator A5043927370 @default.
• W1992295816 creator A5080957799 @default.
• W1992295816 date "2011-01-06" @default.
• W1992295816 modified "2023-09-26" @default.
• W1992295816 title "Tissue-Specific Analysis of Glycogen Synthase Kinase-3α (GSK-3α) in Glucose Metabolism: Effect of Strain Variation" @default.
• W1992295816 cites W1964532167 @default.
• W1992295816 cites W1966373813 @default.
• W1992295816 cites W1980220309 @default.
• W1992295816 cites W1983435458 @default.
• W1992295816 cites W1995856733 @default.
• W1992295816 cites W2001866120 @default.
• W1992295816 cites W2011640487 @default.
• W1992295816 cites W2019041110 @default.
• W1992295816 cites W2026800046 @default.
• W1992295816 cites W2054716401 @default.
• W1992295816 cites W2072556905 @default.
• W1992295816 cites W2079503496 @default.
• W1992295816 cites W2083308747 @default.
• W1992295816 cites W2109479865 @default.
• W1992295816 cites W2117793740 @default.
• W1992295816 cites W2119584760 @default.
• W1992295816 cites W2124867155 @default.
• W1992295816 cites W2125793202 @default.
• W1992295816 cites W2128282944 @default.
• W1992295816 cites W2130357785 @default.
• W1992295816 cites W2139997006 @default.
• W1992295816 cites W2140622624 @default.
• W1992295816 cites W2140664543 @default.
• W1992295816 cites W2145808065 @default.
• W1992295816 cites W2156420000 @default.
• W1992295816 cites W2156788906 @default.
• W1992295816 doi "https://doi.org/10.1371/journal.pone.0015845" @default.
• W1992295816 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3017066" @default.
• W1992295816 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21253590" @default.
• W1992295816 hasPublicationYear "2011" @default.
• W1992295816 type Work @default.
• W1992295816 sameAs 1992295816 @default.
• W1992295816 citedByCount "33" @default.
• W1992295816 countsByYear W19922958162012 @default.
• W1992295816 countsByYear W19922958162013 @default.
• W1992295816 countsByYear W19922958162014 @default.
• W1992295816 countsByYear W19922958162015 @default.
• W1992295816 countsByYear W19922958162016 @default.
• W1992295816 countsByYear W19922958162017 @default.
• W1992295816 countsByYear W19922958162018 @default.
• W1992295816 countsByYear W19922958162019 @default.
• W1992295816 countsByYear W19922958162020 @default.
• W1992295816 countsByYear W19922958162021 @default.
• W1992295816 countsByYear W19922958162022 @default.
• W1992295816 countsByYear W19922958162023 @default.
• W1992295816 crossrefType "journal-article" @default.
• W1992295816 hasAuthorship W1992295816A5033476856 @default.
• W1992295816 hasAuthorship W1992295816A5043927370 @default.
• W1992295816 hasAuthorship W1992295816A5080957799 @default.
• W1992295816 hasBestOaLocation W19922958161 @default.
• W1992295816 hasConcept C126322002 @default.
• W1992295816 hasConcept C134018914 @default.
• W1992295816 hasConcept C17093226 @default.
• W1992295816 hasConcept C182996813 @default.
• W1992295816 hasConcept C184235292 @default.
• W1992295816 hasConcept C192118531 @default.
• W1992295816 hasConcept C2777180221 @default.
• W1992295816 hasConcept C2777391703 @default.
• W1992295816 hasConcept C2777499176 @default.
• W1992295816 hasConcept C2779306644 @default.
• W1992295816 hasConcept C2779959927 @default.
• W1992295816 hasConcept C55493867 @default.
• W1992295816 hasConcept C555293320 @default.
• W1992295816 hasConcept C62231903 @default.
• W1992295816 hasConcept C71924100 @default.
• W1992295816 hasConcept C86803240 @default.
• W1992295816 hasConceptScore W1992295816C126322002 @default.
• W1992295816 hasConceptScore W1992295816C134018914 @default.
• W1992295816 hasConceptScore W1992295816C17093226 @default.
• W1992295816 hasConceptScore W1992295816C182996813 @default.
• W1992295816 hasConceptScore W1992295816C184235292 @default.
• W1992295816 hasConceptScore W1992295816C192118531 @default.
• W1992295816 hasConceptScore W1992295816C2777180221 @default.
• W1992295816 hasConceptScore W1992295816C2777391703 @default.
• W1992295816 hasConceptScore W1992295816C2777499176 @default.
• W1992295816 hasConceptScore W1992295816C2779306644 @default.
• W1992295816 hasConceptScore W1992295816C2779959927 @default.
• W1992295816 hasConceptScore W1992295816C55493867 @default.
• W1992295816 hasConceptScore W1992295816C555293320 @default.
• W1992295816 hasConceptScore W1992295816C62231903 @default.
• W1992295816 hasConceptScore W1992295816C71924100 @default.
• W1992295816 hasConceptScore W1992295816C86803240 @default.
• W1992295816 hasIssue "1" @default.
• W1992295816 hasLocation W19922958161 @default.
• W1992295816 hasLocation W19922958162 @default.
• W1992295816 hasLocation W19922958163 @default.
• W1992295816 hasLocation W19922958164 @default.
• W1992295816 hasLocation W19922958165 @default.
• W1992295816 hasOpenAccess W1992295816 @default.
• W1992295816 hasPrimaryLocation W19922958161 @default.

• next