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地尔硫䓬治疗糖尿病心肌病时的不良代谢效应。

Adverse Metabolic Effects of Diltiazem Treatment During Diabetic Cardiomyopathy.

机构信息

College of Pharmacy, The Ohio State University, OH, USA.

Department of Physiological Sciences, Oklahoma State University, OK, USA.

出版信息

J Cardiovasc Pharmacol Ther. 2019 Mar;24(2):193-203. doi: 10.1177/1074248418808392. Epub 2018 Nov 20.

Abstract

Diabetes is a global epidemic disease, which leads to multiorgan dysfunction, including heart disease. Diabetes results from the limited absorption of glucose into insulin-sensitive tissues. The heart is one of the main organs to utilize glucose as an energy substrate. Glucose uptake into striated muscle is regulated by a family of membrane proteins called glucose transporters (GLUTs). Although calcium channel blockers, including diltiazem, are widely prescribed drugs for cardiovascular diseases, including in patients with diabetes, their pharmacological effects on glucose metabolism are somewhat controversial. We hypothesized that diltiazem treatment will exhibit detrimental effects on whole body glucose homeostasis and glucose transport in the striated muscle of patients with diabetes. Healthy and streptozotocin-treated rats were randomly assigned to receive diltiazem treatment or a placebo for 8 weeks. Blood glucose was significantly increased in the untreated diabetic groups, which worsened after diltiazem treatment. Diabetes decreased protein content of both GLUT4 (the predominate insulin-sensitive glucose transporter) and AS160 (Akt Substrate at 160 kDa, the downstream protein in the signaling cascade that regulates GLUT4 trafficking) in striated muscle of diabetic rats, with a more pronounced alteration after diltiazem treatment. We additionally reported that diabetic rodents displayed marked systolic dysfunction, which was not rescued by diltiazem treatment. In conclusion, diltiazem treatment worsened the effects of diabetes-induced hyperglycemia and diabetes-induced alterations in the regulation of glucose transport in striated muscle.

摘要

糖尿病是一种全球性的流行病,可导致多器官功能障碍,包括心脏病。糖尿病是由于葡萄糖向胰岛素敏感组织的吸收受限所致。心脏是利用葡萄糖作为能量底物的主要器官之一。横纹肌中葡萄糖摄取受称为葡萄糖转运蛋白(GLUTs)的一系列膜蛋白调节。尽管包括地尔硫卓在内的钙通道阻滞剂被广泛用于治疗心血管疾病,包括糖尿病患者,但它们对葡萄糖代谢的药理学作用存在一些争议。我们假设地尔硫卓治疗会对糖尿病患者的全身葡萄糖稳态和横纹肌中的葡萄糖转运产生不利影响。健康和链脲佐菌素处理的大鼠被随机分配接受地尔硫卓治疗或安慰剂治疗 8 周。未经治疗的糖尿病组的血糖显着升高,地尔硫卓治疗后恶化。糖尿病降低了糖尿病大鼠横纹肌中 GLUT4(主要的胰岛素敏感葡萄糖转运蛋白)和 AS160(Akt 底物 160 kDa,调节 GLUT4 转运的信号级联中的下游蛋白)的蛋白含量,地尔硫卓治疗后更明显。我们还报告说,糖尿病啮齿动物表现出明显的收缩功能障碍,地尔硫卓治疗未能挽救这种障碍。总之,地尔硫卓治疗加重了糖尿病引起的高血糖和糖尿病引起的横纹肌葡萄糖转运调节改变的影响。

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