Adiponectin receptor 1 overexpression reduces lipid accumulation and hypertrophy in the heart of diet-induced obese mice--possible involvement of oxidative stress and autophagy.

BACKGROUND

Studies show that adiponectin and its receptors (AdipoR1 and 2) play important roles in regulating glucose and lipid metabolism in mice. Obesity, type II diabetes and cardiovascular disease are highly correlated with downregulated adiponectin signaling; however, research has not clarified the functions of AdipoR1 in vivo.

METHODS

In this study, mice were induced to overexpress the AdipoR1 transgene so that its functions could be studied in relation to hypertrophic cardiomyopathy. Wild-type and AdipoR1-transgenic male mice were fed ad libitum with a standard chow diet or else a high-fat/sucrose diet (HFSD) for 24 weeks, beginning at 6-7 weeks of age.

RESULTS

After receiving the 24-week HFSD, AdipoR1-transgenic mice did not become obese, nor did they develop heart hypertrophy. The AdipoR1 transgene decreased the elevating cardiac troponin I expression caused by the HFSD. While the HFSD induced mRNA expression of CD36 and CPTI, AdipoR1 reversed it. Suppression of cardiac SOD mRNA expression by the HFSD was improved by the AdipoR1 transgene. The HFSD caused a higher autophagic gene expression of Beclin 1 and Lamp 2 A in the heart, whereas the AdipoR1 transgene ameliorated them.

CONCLUSIONS

The AdipoR1 transgene enabled mice to resist diet-induced obesity while decreasing lipid accumulation, oxidative stress and autophagic damage. These effects might contribute to the improvement of heart functions in diet-induced obese mice.