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. 2019 Mar 1;7(4):763–781. doi: 10.1016/j.jcmgh.2019.02.002

Figure 9.

Figure 9

LPGAT1 deficiency impaired insulin signaling. (A) Subcellular fractionation analysis of LPGAT1 stably expressed in COS-7 cells. Calnexin was blotted as an endoplasmic reticulum marker. (B–D) Western blot analysis of insulin-stimulated phosphorylation of Akt and Gsk3α/β in different metabolic tissues isolated from LPGAT1-/- and WT control mice, including (B) liver, (E) primary hepatocytes in culture, (F) skeletal muscle, and (G) heart. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as internal control for protein loading. Mice were fasted for 12 hours and then stimulated with insulin (1 U/kg body weight) for 15 minutes. Primary hepatocytes were stimulated with the indicated concentrations of insulin for 15 minutes. (C and D) Quantification of the phosphorylation level of (C) Akt and (D) Gsk3α in the liver by ImageJ (National Institutes of Health, Bethesda, MD). Data are representative of 3 independent experiments, and represented as means ± SD (n = 3). *P < .05 by 1-way analysis of variance. Ctrl, control; KO, knockout; Sk, skeletal.