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Obesity induces upregulation of genes involved in myocardial Ca2+ handling

机译:肥胖引起心肌钙离子处理相关基因的上调

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Obesity is a complex multifactorial disorder that is often associated with cardiovascular diseases. Research on experimental models has suggested that cardiac dysfunction in obesity might be related to alterations in myocardial intracellular calcium (Ca2+) handling. However, information about the expression of Ca2+-related genes that lead to this abnormality is scarce. We evaluated the effects of obesity induced by a high-fat diet in the expression of Ca2+-related genes, focusing the L-type Ca2+ channel (Cacna1c), sarcolemmal Na+/Ca2+ exchanger (NCX), sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), ryanodine receptor (RyR2), and phospholamban (PLB) mRNA in rat myocardium. Male 30-day-old Wistar rats were fed a standard (control) or high-fat diet (obese) for 15 weeks. Obesity was defined as increased percent of body fat in carcass. The mRNA expression of Ca2+-related genes in the left ventricle was measured by RT-PCR. Compared with control rats, the obese rats had increased percent of body fat, area under the curve for glucose, and leptin and insulin plasma concentrations. Obesity also caused an increase in the levels of SERCA2a, RyR2 and PLB mRNA (P < 0.05) but did not modify the mRNA levels of Cacna1c and NCX. These findings show that obesity induced by high-fat diet causes cardiac upregulation of Ca2+ transport_related genes in the sarcoplasmic reticulum.
机译:肥胖是一种复杂的多因素疾病,通常与心血管疾病有关。对实验模型的研究表明,肥胖症中的心脏功能障碍可能与心肌细胞内钙(Ca2 +)处理的改变有关。但是,关于导致这种异常的Ca 2+相关基因的表达的信息很少。我们评估了高脂饮食诱导的肥胖对Ca2 +相关基因表达的影响,重点研究了L型Ca2 +通道(Cacna1c),肌膜Na + / Ca2 +交换子(NCX),肌浆网Ca2 + ATPase(SERCA2a),大鼠心肌中的ryanodine受体(RyR2)和phosphorlamban(PLB)mRNA。对30天大的Wistar大鼠进行标准(对照)或高脂饮食(肥胖)喂养15周。肥胖被定义为car体中体内脂肪增加的百分比。用RT-PCR检测左心室Ca2 +相关基因的mRNA表达。与对照组相比,肥胖大鼠的体脂百分比,葡萄糖曲线下面积,瘦素和胰岛素血浆浓度增加。肥胖也引起SERCA2a,RyR2和PLB mRNA的水平升高(P <0.05),但并未改变Cacna1c和NCX的mRNA水平。这些发现表明,高脂饮食诱导的肥胖会导致肌浆网中Ca2 +转运相关基因的心脏上调。

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