Abstract

This study is aimed to explore the effect of improved insulin sensitivity on the expression of apolipoprotein M (ApoM). Primary hepatocytes and skeletal myocytes of ApoM knockout (ApoM-/-) mouse were transfected with lentivirus vector containing the human ApoM gene (LV-ApoM), and an empty vector was used as a control group (LV-Ctrl). JNK inhibitor, SP600125 was added to improve the insulin sensitivity of cells. After 18h of cultivation, the cells were collected after stimulation with 100nM. insulin for 30min. The expression levels of ApoM and JNK1 mRNA were detected by real-time PCR, while the expression of phosphorylate protein kinase B (p-AKT) was assessed by Western blot analysis. The results showed that enhancement of insulin signaling pathway by SP600125 significantly increased ApoM mRNA expression and ApoM overexpression significantly elevated the protein level of p-AKT in primary skeletal myocytes, which indicated that increased insulin sensitivity could promote the expression of ApoM and ApoM overexpression could also promote the activation of insulin signaling pathway.

Keywords: Apolipoprotein M (ApoM); Type 2 diabetes; Hepatocytes; Skeletal myocytes; Insulin

Abbreviations: ApoM: Apolipoprotein M; HDL: High Density Lipoprotein; PBS: Phosphate Buffer Saline; PAS: Periodic Acid-Schiff; GFP: Green Fluorescent Protein; GAPDH: Glyceraldehyde 3-Phosphate Dehydrogenase