Irisin protects against ischemia/reperfusion injury to the lung by improving mitochondrial function.

Epicardial fat tissue (EFT) is the visceral fat distributed along the coronary arteries between the pericardium and the myocardium. Increases in EFT are closely related to the occurrence of diabetes mellitus (DM) and cardiovascular disease. To further understand the link between EFT and DM, we conducted a meta-analysis of the relevant literature. We systematically searched electronic databases for studies on EFT performed in DM patients and published up to 30 September 2018. We included data on EFT in a DM patient group and a non-DM control group. We then assessed the effect of DM on EFT by meta-analysis and trial sequential analysis (TSA). All statistical analyses were performed using Stata 12.0 and TSA software. A total of 13 studies (n = 1102 patients) were included in the final analysis. Compared with the control group, DM patients had significantly higher EFT (SMD: 1.23; 95% CI 0.98, 1.48; P = 0.000; TSA-adjusted 95% CI 0.91, 2.13; P < 0.0001). The TSA indicated that the available samples were sufficient and confirmed that firm evidence was reached. According to the regression analysis and subgroup analyses, DM typing, EFT ultrasound measurements, total cholesterol (TC) and triglyceride (TG) levels were confounding factors that significantly affected our results. Our meta-analysis suggests that the amount of EFT is significantly higher in DM patients than in non-DM patients.

Cardiac hypertrophy is accompanied by increased myocardial oxidative stress, and whether naringenin, a natural antioxidant, is effective in the therapy of cardiac hypertrophy remains unknown. In the present study, different dosage regimens (25, 50, and 100 mg/kg/d for three weeks) of naringenin (NAR) were orally gavaged in an isoprenaline (ISO) (7.5mg/kg)-induced cardiac hypertrophic C57BL/6J mouse model. The administration of ISO led to significant cardiac hypertrophy, which was alleviated by pretreatment with naringenin in both in vivo and in vitro experiments. Naringenin inhibited ISO-induced oxidative stress, as demonstrated by the increased SOD activity, decreased MDA level and NOX2 expression, and inhibited MAPK signaling. Meanwhile, after the pretreatment with compound C (a selective AMPK inhibitor), the anti-hypertrophic and anti-oxidative stress effects of naringenin were blocked, suggesting the protective effect of naringenin on cardiac hypertrophy. Our present study indicated that naringenin attenuated ISO-induced cardiac hypertrophy by regulating the AMPK/NOX2/MAPK signaling pathway.