Single phosphorylation sites in Acc1 and Acc2 regulate lipid homeostasis and the insulin–sensitizing

Hfdfed wt and dki n 12 wt and 16 dki hfdmetformin the

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HFD–fed WT and DKI; n = 12 WT and 16 DKI HFD–metformin). The effect of metformin treatment on ( c ) hepatic glucose production (HGP) and ( d ) suppression of HGP by insulin ( n = 7 WT and 9 DKI). ( e ) Akt (Ser473) and FoxO1 (Ser253) phosphorylation, as well as ( f ) G6p and Pck expression, in isolated hepatocytes treated with chronic palmitate (18 h) and stimulated with insulin, where gene expression is shown relative to the WT condition without palmitate. ( g ) Hepatic glucose production, following chronic (18 h) exposure to palmitate (0.5 mM) in the presence or absence of metformin (0.5 mM), then in response to Bt 2 –cAMP (100 μM) and insulin (10 nM) for 4 h, in the absence of acute metformin. ( n = 3, from at least 3 separate experiments). Hatched line represents control hepatocytes not stimulated with Bt 2 –cAMP for glucose production. ( h ) Schematic representation of metformin’s therapeutic effects on hepatic action during differential nutrient and hormonal programs. Data are expressed as means ± SEM, * P < 0.05, ** P < 0.01 and *** P < 0.001 represent differences between genotype and # P < 0.05, ## P < 0.01 and ### P < 0.001 are differences between treatment, as calculated by two–way ANOVA and Bonferonni post hoc test. Fullerton et al. Page 16 Nat Med . Author manuscript; available in PMC 2016 July 28. CIHR Author Manuscript CIHR Author Manuscript CIHR Author Manuscript
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  • Winter '19
  • Robert S Kiss
  • Insulin resistance, Fatty acid metabolism

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