Durak Aysegul, Olgar Yusuf, Tuncay Erkan, Karaomerlioglu Irem, Kayki Mutlu Gizem, Arioglu Inan Ebru, Altan Vecdi Melih, Turan Belma
a Department of Biophysics, Faculty of Medicine, Ankara University, Ankara, Turkey.
b Department of Pharmacology, Faculty of Pharmacy, Ankara University, Ankara, Turkey.
Can J Physiol Pharmacol. 2017 Nov;95(11):1335-1342. doi: 10.1139/cjpp-2017-0054. Epub 2017 Jul 30.
Mechanical activity of the heart is adversely affected in metabolic syndrome (MetS) characterized by increased body mass and marked insulin resistance. Herein, we examined the effects of high carbohydrate intake on cardiac function abnormalities by evaluating in situ heart work, heart rate, and electrocardiograms (ECGs) in rats. MetS was induced in male Wistar rats by adding 32% sucrose to drinking water for 22-24 weeks and was confirmed by insulin resistance, increased body weight, increased blood glucose and serum insulin, and increased systolic and diastolic blood pressures in addition to significant loss of left ventricular integrity and increased connective tissue around myofibrils. Analysis of in situ ECG recordings showed a markedly shortened QT interval and decreased QRS amplitude with increased heart rate. We also observed increased oxidative stress and decreased antioxidant defense characterized by decreases in serum total thiol level and attenuated paraoxonase and arylesterase activities. Our data indicate that increased heart rate and a shortened QT interval concomitant with higher left ventricular developed pressure in response to β-adrenoreceptor stimulation as a result of less cyclic AMP release could be regarded as a natural compensation mechanism in overweight rats with MetS. In addition to the persistent insulin resistance and obesity associated with MetS, one should consider the decreased heart work, increased heart rate, and shortened QT interval associated with high carbohydrate intake, which may have more deleterious effects on the mammalian heart.
以体重增加和显著胰岛素抵抗为特征的代谢综合征(MetS)会对心脏的机械活动产生不利影响。在此,我们通过评估大鼠的原位心脏做功、心率和心电图(ECG),研究了高碳水化合物摄入对心脏功能异常的影响。通过在雄性Wistar大鼠饮用水中添加32%的蔗糖22 - 24周来诱导MetS,除了左心室完整性显著丧失和肌原纤维周围结缔组织增加外,还通过胰岛素抵抗、体重增加、血糖和血清胰岛素升高以及收缩压和舒张压升高来确认。对原位心电图记录的分析显示,随着心率增加,QT间期明显缩短,QRS波幅降低。我们还观察到氧化应激增加和抗氧化防御降低,表现为血清总硫醇水平降低以及对氧磷酶和芳基酯酶活性减弱。我们的数据表明,由于环磷酸腺苷释放减少,对β - 肾上腺素能受体刺激的反应中,心率增加和QT间期缩短伴随着更高的左心室舒张末压,这可被视为患有MetS的超重大鼠的一种自然补偿机制。除了与MetS相关的持续胰岛素抵抗和肥胖外,还应考虑与高碳水化合物摄入相关的心脏做功减少、心率增加和QT间期缩短,这可能对哺乳动物心脏产生更有害的影响。