Abstract
The aim of the present study was to explore the association between apolipoprotein M (ApoM) and adiponectin, and the underlying mechanism, via observation of ApoM expression in an obese mouse model. For in vivo experiments, mice were randomly distributed into four groups: Control group, obese group, obese group treated with adiponectin, and normal group treated with adiponectin. Body weight, plasma adiponectin, blood glucose and fasting insulin were measured and visceral adipose tissue was weighed at the end of the experiment. ApoM and transcription factor forkhead box A2 (Foxa2) mRNA expression in the mouse liver was evaluated and the protein level of ApoM detected. For in vitro experiments, an insulin-resistant (IR) hepatic cell model was established by inducing the HepG2 cell line with a high concentration of insulin. Following treatment with adiponectin, changes in ApoM and Foxa2 mRNA expression and ApoM protein expression were evaluated in the control and IR HepG2 cells. Results demonstrated that compared with the control group, body weight, visceral adipose tissue weight, blood glucose, fasting insulin and insulin-resistance index (HOMA-IR) were significantly increased in the obese group, whilst plasma adiponectin, ApoM mRNA expression, Foxa2 mRNA expression and ApoM protein in the mouse liver were all significantly decreased. Following intervention with adiponectin in obese mice, blood glucose, insulin and HOMA-IR were significantly decreased, whilst plasma adiponectin, ApoM mRNA expression, Foxa2 mRNA expression and ApoM protein were all significantly increased. However, no significant difference was observed in visceral adipose tissue weight following the intervention of adiponectin in obese mice. In vitro, in the absence of intervention, ApoM and Foxa2 mRNA expression and ApoM protein expression were significantly lower in IR HepG2 cells compared with HepG2 cells. Following intervention with adiponectin on IR HepG2 cells, ApoM and Foxa2 mRNA expression and ApoM protein expression were significantly increased. However, the intervention did not have any effect on HepG2 cells. In conclusion, intervention with adiponectin elevated ApoM mRNA expression, potentially via relieving IR and upregulating Foxa2 mRNA expression.