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首页> 外文期刊>Physiological Reports >Moderate exercise training does not prevent the reduction in myocardial L?¢????type Ca 2+ channels protein expression at obese rats
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Moderate exercise training does not prevent the reduction in myocardial L?¢????type Ca 2+ channels protein expression at obese rats

机译:适度的运动训练不能阻止肥胖大鼠心肌Lαβ?型Ca 2+通道蛋白表达的降低

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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,肥胖症牵涉与心肌Lαββ型钙通道(LTCCs)活动障碍有关的心脏功能障碍,以及适度运动训练(MET)似乎是重要的治疗手段。我们测试了以下假设,即MET可促进由不饱和高脂肪饮食引起的肥胖症患者对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),该大鼠接受标准饮食并肥胖(Ob; n ???? = ???? 40),哪些接受了高脂肪饮食。 20周后,将动物分为四组:对照组(C;n≤25= 12);对照组(C = n = 12)。控制提交锻炼训练(ET; n = 14 = 14);肥胖的(Ob; n ???? = ???? 10);和肥胖者接受运动训练(ObET; n = 11 = 11)。 ET(第12周的每周5周/天)在第21周开始,跑步机的运行逐渐增加到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评估LTCC的蛋白表达。在所有实验方案中,不饱和高脂肪饮食都会促进肥胖。 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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