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Moderate exercise training does not prevent the reduction in myocardial L‐type Ca2+ channels protein expression at obese rats

机译:中等运动训练不能阻止肥胖大鼠心肌L型Ca2 +通道蛋白表达的减少

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摘要

Authors have showed that obesity implicates cardiac dysfunction associated with myocardial L‐type calcium channels (LTCCs) activity impairments, as well as moderate exercise training (MET) seems to be an important therapeutic tool. We tested the hypothesis that MET promotes improvements on LTCCS activity and protein expression at obesity induced by unsaturated high‐fat diets, which could represent a protective effects against development of cardiovascular damage. Male Wistar rats were randomized in control (C, n = 40), which received a standard diet and obese (Ob; n = 40), which received high‐fat diet. After 20 weeks, the animals were assigned at four groups: control (C; n = 12); control submitted to exercise training (ET; n = 14); obese (Ob; n = 10); and obese submitted to exercise training (ObET; n = 11). ET (5 days/week during 12 weeks) began in the 21th week and consisted of treadmill running that was progressively increased to reach 60 min. Final body weight (FBW), body fat (BF), adiposity index (AI), comorbidities, and hormones were evaluated. Cardiac remodeling was assessed by morphological and isolated papillary muscles function. LTCCs activity was determined using specific blocker, while protein expression of LTCCs was evaluated by Western blot. Unsaturated high‐fat diet promoted obesity during all experimental protocol. MET controlled obesity process by decreasing of FBW, BF, and AI. Obesity implicated to LTCCs protein expression reduction and MET was not effective to prevent this condition. ET was efficient to promote several improvements to body composition and metabolic parameters; however, it was not able to prevent or reverse the downregulation of LTCCs protein expression at obese rats.
机译:作者已经表明,肥胖与心肌L型钙通道(LTCCs)活动障碍相关的心脏功能障碍有关,而中等运动训练(MET)似乎是一种重要的治疗手段。我们测试了以下假设:MET促进了由不饱和高脂饮食诱导的肥胖症患者LTCCS活性和蛋白质表达的改善,这可能代表了对心血管损害发展的保护作用。将雄性Wistar大鼠随机分为对照组(C,n = 40)和肥胖(Ob; n = 40),后者接受高脂饮食。 20周后,将动物分为四组:对照组(C; n = 12);接受运动训练的控制(ET; n = 14);肥胖(Ob; n = 10);和肥胖者接受运动训练(ObET; n = 11)。 ET(在12周内每周5天/周)从第21周开始,包括跑步机运行,逐渐增加到60分钟。评估了最终体重(FBW),体脂(BF),肥胖指数(AI),合并症和激素。通过形态学和孤立的乳头肌功能评估心脏重塑。使用特异性阻断剂确定LTCC的活性,同时通过蛋白质印迹法评估LTCC的蛋白表达。在所有实验方案中,不饱和高脂饮食都会促进肥胖。 MET通过减少FBW,BF和AI控制肥胖症过程。肥胖与LTCCs蛋白表达降低有关,而MET不能有效地预防这种情况。 ET可以有效促进人体成分和代谢参数的多种改善。但是,它不能预防或逆转肥胖大鼠LTCCs蛋白表达的下调。

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