CD36/Sirtuin 1 Axis Impairment Contributes to Hepatic Steatosis in ACE2-Deficient Mice

Figure 5

Hepatic glucose metabolism. (a) Evaluation of hepatic gluconeogenesis stimulated by intraperitoneal injection of pyruvate and area under the curve of the test (AUC); (b) relative mRNA expression of glycolytic genes in the liver (glucokinase, GCK; glucose 6-phosphatase, G6Pase; phosphoenolpyruvate carboxykinase 1 and 2, PCK; insulin receptor, IR; and glucose transporter type 2, GLUT2) (arbitrary units); (c) α-insulin receptor substrate-1 (αIRS) protein expression in the liver (arbitrary units); (d) phosphatidyl inositol-3 kinase (PI3-K) protein expression in the liver (arbitrary units); (e) AKT protein expression in the liver (arbitrary units); (f) glycogen synthase kinase (GSK) 3β in the liver (arbitrary units); (g) phospho-GSK 3β in the liver (arbitrary units); (h) GSK 3β/phospho-GSK 3β in the liver (arbitrary units) of WT and ACE2 mice at the age of 6 months. Data are presented as mean ± SEM. Student’s test: ; ; .

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