Matches in SemOpenAlex for { <https://semopenalex.org/work/W2071068196> ?p ?o ?g. }
- W2071068196 endingPage "800" @default.
- W2071068196 startingPage "791" @default.
- W2071068196 abstract "Chronic hyperglycemia and inflammatory cytokines disrupt and/or attenuate signal transduction pathways that promote normal β-cell survival, leading to the destruction of endocrine pancreas in type 2 diabetes. There is convincing evidence that autocrine insulin signalling exerts protective anti-apoptotic effects on beta cells. Suppressors of cytokine signalling (SOCS) were induced by several cytokines and inhibit insulin-initiated signal transduction. The aim of this study was to investigate whether high glucose can influence endogenous interleukin-1β (IL-1β) and SOCS expression thus affecting insulin signalling and survival in insulin-producing mouse pancreatic beta cells (βTC-6). Results showed that prolonged exposure of βTC-6 cells to increased glucose concentrations resulted in significant inhibition of insulin-induced tyrosine phosphorylation of the insulin receptor (IR), and insulin receptor substrate-2 (IRS-2) as well as PI3-kinase activation. These changes were accompanied by impaired activation of the anti-apoptotic signalling protein Akt and annulment of Akt-mediated suppression of the Forkhead family of transcription factors (FoxO) activation. Glucose-induced attenuation of IRS-2/Akt-mediated signalling was associated with increased IL-1β expression. Enhanced endogenous IL-1β specifically induced mRNA and protein expression of SOCS-1 in βTC-6 cells. Inhibition of SOCS-1 expression by SOCS-1-specific small interfering RNA restored IRS-2/PI3K-mediated Akt phosphorylation suppressed by high glucose. The upregulation of endogenous cytokine signalling and FoxO activation were accompanied by enhanced caspase-3 activation and increased susceptibility of cells to apoptosis. These results indicated that glucose-induced endogenous IL-1β expression increased βTC-6 cells apoptosis by inhibiting, at least in part, IRS-2/Akt-mediated signalling through SOCS-1 upregulation." @default.
- W2071068196 created "2016-06-24" @default.
- W2071068196 creator A5006641296 @default.
- W2071068196 creator A5006806405 @default.
- W2071068196 creator A5046811448 @default.
- W2071068196 creator A5085557707 @default.
- W2071068196 creator A5091896059 @default.
- W2071068196 date "2010-05-01" @default.
- W2071068196 modified "2023-10-17" @default.
- W2071068196 title "High glucose induces suppression of insulin signalling and apoptosis via upregulation of endogenous IL-1β and suppressor of cytokine signalling-1 in mouse pancreatic beta cells" @default.
- W2071068196 cites W1543408750 @default.
- W2071068196 cites W1556383867 @default.
- W2071068196 cites W1624505911 @default.
- W2071068196 cites W1697523131 @default.
- W2071068196 cites W1794038664 @default.
- W2071068196 cites W1964466523 @default.
- W2071068196 cites W1964832108 @default.
- W2071068196 cites W1966977991 @default.
- W2071068196 cites W1968646619 @default.
- W2071068196 cites W1983513002 @default.
- W2071068196 cites W1987265109 @default.
- W2071068196 cites W1991777822 @default.
- W2071068196 cites W1991917446 @default.
- W2071068196 cites W1995646241 @default.
- W2071068196 cites W1998002161 @default.
- W2071068196 cites W2005913547 @default.
- W2071068196 cites W2013427376 @default.
- W2071068196 cites W2021806225 @default.
- W2071068196 cites W2024992738 @default.
- W2071068196 cites W2029870728 @default.
- W2071068196 cites W2033726443 @default.
- W2071068196 cites W2040692229 @default.
- W2071068196 cites W2050720508 @default.
- W2071068196 cites W2069711307 @default.
- W2071068196 cites W2079797384 @default.
- W2071068196 cites W2080999576 @default.
- W2071068196 cites W2088430561 @default.
- W2071068196 cites W2105584844 @default.
- W2071068196 cites W2107232633 @default.
- W2071068196 cites W2108768245 @default.
- W2071068196 cites W2111128761 @default.
- W2071068196 cites W2112115574 @default.
- W2071068196 cites W2115240185 @default.
- W2071068196 cites W2115723208 @default.
- W2071068196 cites W2117028091 @default.
- W2071068196 cites W2126295203 @default.
- W2071068196 cites W2126393987 @default.
- W2071068196 cites W2130078845 @default.
- W2071068196 cites W2132227356 @default.
- W2071068196 cites W2137035181 @default.
- W2071068196 cites W2139940038 @default.
- W2071068196 cites W2140793658 @default.
- W2071068196 cites W2146272458 @default.
- W2071068196 cites W2146561547 @default.
- W2071068196 cites W2146921827 @default.
- W2071068196 cites W2151634661 @default.
- W2071068196 cites W2153977812 @default.
- W2071068196 cites W2157518285 @default.
- W2071068196 cites W2164691388 @default.
- W2071068196 cites W2166099437 @default.
- W2071068196 cites W2166998858 @default.
- W2071068196 cites W4242514389 @default.
- W2071068196 doi "https://doi.org/10.1016/j.cellsig.2010.01.003" @default.
- W2071068196 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20067833" @default.
- W2071068196 hasPublicationYear "2010" @default.
- W2071068196 type Work @default.
- W2071068196 sameAs 2071068196 @default.
- W2071068196 citedByCount "42" @default.
- W2071068196 countsByYear W20710681962012 @default.
- W2071068196 countsByYear W20710681962013 @default.
- W2071068196 countsByYear W20710681962014 @default.
- W2071068196 countsByYear W20710681962015 @default.
- W2071068196 countsByYear W20710681962016 @default.
- W2071068196 countsByYear W20710681962017 @default.
- W2071068196 countsByYear W20710681962018 @default.
- W2071068196 countsByYear W20710681962019 @default.
- W2071068196 countsByYear W20710681962020 @default.
- W2071068196 crossrefType "journal-article" @default.
- W2071068196 hasAuthorship W2071068196A5006641296 @default.
- W2071068196 hasAuthorship W2071068196A5006806405 @default.
- W2071068196 hasAuthorship W2071068196A5046811448 @default.
- W2071068196 hasAuthorship W2071068196A5085557707 @default.
- W2071068196 hasAuthorship W2071068196A5091896059 @default.
- W2071068196 hasConcept C104317684 @default.
- W2071068196 hasConcept C112446052 @default.
- W2071068196 hasConcept C126042315 @default.
- W2071068196 hasConcept C126322002 @default.
- W2071068196 hasConcept C127561419 @default.
- W2071068196 hasConcept C128240485 @default.
- W2071068196 hasConcept C134018914 @default.
- W2071068196 hasConcept C162354598 @default.
- W2071068196 hasConcept C170493617 @default.
- W2071068196 hasConcept C185592680 @default.
- W2071068196 hasConcept C203014093 @default.
- W2071068196 hasConcept C2777391703 @default.
- W2071068196 hasConcept C2778690821 @default.
- W2071068196 hasConcept C2778923194 @default.
- W2071068196 hasConcept C2779306644 @default.