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Expression of apolipoprotein M and its association with adiponectin in an obese mouse model
Liu Yang1, Tie Li2, Shuiping Zhao3
1International Medical Center, Geriatric Department, National Clinical Research Center of Geriatric Diseases, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
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.
Insights
Adiponectin treatment increased apolipoprotein M (ApoM) expression in obese mice and insulin-resistant cells. This suggests adiponectin may help regulate ApoM levels by improving insulin resistance and boosting Foxa2 expression.
Area of Science:
- Metabolic research
- Endocrinology
- Molecular biology
Background:
- Obesity is linked to altered levels of adipokines like adiponectin and apolipoprotein M (ApoM).
- The relationship between adiponectin and ApoM, particularly in the context of obesity and insulin resistance, requires further elucidation.
- Understanding these molecular interactions is crucial for developing therapeutic strategies targeting metabolic disorders.
Purpose of the Study:
- To investigate the association between adiponectin and apolipoprotein M (ApoM) in an obese mouse model.
- To explore the underlying molecular mechanisms, including the role of transcription factor Foxa2.
- To examine the effects of adiponectin intervention on ApoM expression in both in vivo and in vitro models of insulin resistance.
Main Methods:
- In vivo: Obese mice were treated with adiponectin; body weight, plasma adiponectin, glucose, insulin, and visceral adipose tissue were measured. Liver ApoM and Foxa2 mRNA and protein levels were assessed.
- In vitro: An insulin-resistant (IR) HepG2 cell model was established and treated with adiponectin. Changes in ApoM and Foxa2 mRNA and ApoM protein expression were evaluated.
Main Results:
- Obese mice exhibited increased body weight, visceral fat, glucose, insulin, and HOMA-IR, with decreased plasma adiponectin, liver ApoM, and Foxa2 mRNA.
- Adiponectin treatment in obese mice reduced glucose, insulin, and HOMA-IR, while increasing plasma adiponectin, liver ApoM, and Foxa2 mRNA, but did not significantly alter visceral fat weight.
- In vitro, insulin-resistant HepG2 cells showed lower ApoM and Foxa2 mRNA and ApoM protein expression, which were upregulated by adiponectin treatment.
Conclusions:
- Adiponectin intervention effectively increased ApoM mRNA and protein expression in both obese mice and insulin-resistant hepatic cells.
- The findings suggest that adiponectin may elevate ApoM expression by ameliorating insulin resistance and upregulating Foxa2 mRNA.
- This study highlights a potential molecular pathway involving adiponectin, Foxa2, and ApoM in metabolic regulation.
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