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The molecular causes of type 2 diabetes (T2D) are not well understood. Both type 1 diabetes (T1D) and T2D are characterized by impaired insulin signaling and hyperglycemia. From analogy to T1D, insulin resistance and hyperglycemia are thought to also play causal roles in T2D. Recent clinical studies, however, found that T2D patients treated to maintain glycemia below the diabetes definition threshold (HbA1c < 6.5%) still develop diabetic complications. This suggests additional insulin- and glucose-independent mechanisms could be involved in T2D progression and/or initiation. T2D patients have elevated levels of the metabolite methylglyoxal (MG). We show here, using Drosophila glyoxalase 1 knockouts, that animals with elevated methylglyoxal recapitulate several core aspects of T2D: insulin resistance, obesity, and hyperglycemia. Thus elevated MG could constitute one root cause of T2D, suggesting that the molecular causes of elevated MG warrant further study.
Pubmed ID: 29551588 RIS Download
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This monoclonal targets FLAG
View all literature mentionsThis polyclonal targets Phospho-Drosophila Akt (Ser505)
View all literature mentionsThis polyclonal targets Drosophila p70 S6 Kinase, phospho (Thr398)
View all literature mentionsThis unknown targets Mouse tubulin (alpha-)
View all literature mentionsThis polyclonal targets GLO1
View all literature mentionsDrosophila melanogaster with name w[*]; P{w[+mW.hs]=GAL4-da.G32}UH1, Sb[1]/TM6B, Tb[1] from BDSC.
View all literature mentionsDrosophila melanogaster with name w[1118] from BDSC.
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