Figure 7.

The systematic insulin sensitivity in HFD/STZ mice is improved by hepatic NGBR overexpression. Skeletal muscle samples were collected from mice used in Figure 2A, and the following assays were conducted. A, expressions of p-AKT, AKT, p-GSK3β, GSK3β, NGBR, and β-actin protein were determined by western blot. B–D, expressions of mRNA for genes related to endoplasmic reticulum stress: activating transcription factor 4/6 (Atf4/6), X-box binding protein 1 (Xbp1s), binding immunoglobulin protein (Bip), and DNA-damage inducible transcript 3 (Chop) or mitochondrial functions: peroxisome proliferator-activated receptor-γ coactivator 1α (Pgc1α), sirtuin 1 (Sirt1), mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), optic atrophy (Opa1), dynamin-related protein 1 (Drp1), mitochondrial fission 1 (Fis1), mitochondrial fission factor (Mff), Parkin, and (PTEN)-induced putative kinase 1 (Pink1) were determined by qPCR. ∗p < 0.05 versus NC; ^†p < 0.05 versus T2D; n = 5 (NC group), n = 7 (T2D or T2D+NGBR group).