High-intensity interval training (HIIT) effectively enhances heart function via miR-195 dependent cardiomyopathy reduction in high-fat high-fructose diet-induced diabetic rats
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Authors: Khakdan, Soheyla; Delfan, Maryam; Meymeh, Maryam Heydarpour; Kazerouni, Faranak; Ghaedi, Hamid; Shanaki, Mehrnoosh; Kalaki-Jouybari, Fatemeh; Gorgani-Firuzjaee, Sattar; Rahimipour, Ali
Abstract
Aims:Regarding the fact that up-regulation of miR-195 in diabetic hearts has a potential role in diabetic cardiomyopathy, the present study investigated whether continuous endurance training (CET) and high-intensity interval training (HIIT) reduces miR-195 expression and which exercise is effective in this regard. Methods:Diabetes was induced by high-fat high-fructose diet (HFHFD). Then, the rats were sub-divided into three categories; sedentary (HFHFD + SED), continuous endurance training (HFHFD + CET), and high-intensity interval training group (HFHFD + HIIT). After eight weeks of running, expression of miR-195 and myocardial function were evaluated. Results:HIIT effectively decreases the expression of miR-195 and increases the expression of Sirt1 and BCL-2 in diabetic rats compared with CET. Our results showed that HIIT compared with CET increases left ventricular ejection fraction (LVEF%) and fractional shortening (FS%). Conclusions:Our results indicated that exercise, especially HIIT is an appropriate strategy for reducing miR-195 and improving myocardial function in diabetic rats compared with CET.
Pyrazolone derivative C29 protects against HFD-induced obesity in mice via activation of AMPK in adipose tissue
ACTA PHARMACOLOGICA SINICA
Authors: Li, Bo-han; Zhang, Mei; Duan, Ya-nan; Shuai, Lin; Jiang, Hao-wen; Li, Jia; Nan, Fa-jun; Li, Jing-ya
Abstract
Beige adipocytes have been considered as a potential strategy in anti-obesity therapy because of its thermogenic capacity. AMP-activated protein kinase (AMPK) plays important roles in regulating adipose tissue function. C29 is a novel pyrazolone derivative with AMPK activity. In the current study, we investigated the role of C29 in the regulation of thermogenesis using differentiated adipocytes and diet-induced obese mice, and explored the mechanisms that might be involved in energy expenditure via adipocyte AMPK activation. We showed that treatment with C29 (2.5-10 mu M) concentration-dependently increased thermogenesis in differentiated preadipocytes separated from inguinal white adipose tissue (iWAT), evidenced by increased expression levels of thermogenesis markers such asUcp1,Pgc-1 alpha,Dio2,Prdm16,Cox7a1,Cox8b,Elovl3,andCidea, fatty acid oxidation (FAO) genes includingCpt1a,LcadandPpar alpha, as well as beige-selective genes such asCd137,Tmem26,Slc27a1,andTbx1. In high-fat diet (HFD)-fed mice, oral administration of C29 (30 mg center dot kg(-1)center dot day(-1)) for 9 weeks alleviated HFD-induced obesity, promoted energy expenditure and modulated iWAT browning. However, these effects were not observed in adipose-specific AMPK alpha 1/alpha 2 knockout (AKO) mice following C29 administration. Together, this study demonstrates that C29 regulates energy balance via adipocyte AMPK. Our findings show that the discovery of AMPK activators that specifically target adipose tissue may have therapeutic potential for treating obesity-related metabolic diseases.