Exercise training enhances coronary smooth muscle cell sodium-calcium exchange activity in diabetic dyslipidemic Yucatan swine.
Exercise training enhances coronary smooth muscle cell sodium-calcium exchange activity in diabetic dyslipidemic Yucatan swine.
复制标题
运动训练增强糖尿病血脂异常尤卡坦猪冠状动脉平滑肌细胞钠钙交换活性。
DOI：
10.1111/j.1749-6632.2002.tb04756.x
复制
发表时间：
2002
影响因子：
5.2
通讯作者：
Sturek,M
中科院分区：
文献类型：
--
作者：
Mokelke,EA;Wang,M;Sturek,M
钙（Ca2+）在血管平滑肌细胞中的调节在膜水平上受到通道、泵和交换器的严格控制。这些Ca2+调节机制的功能或数量的任何扰动都可能潜在地改变内流和外排之间的平衡，最终导致Ca2+储存过载或细胞质或核Ca2+升高。糖尿病1、2和运动3都被证明可以独立地改变血管平滑肌Ca2+调节的成分。我们在尤卡坦微型猪模型中验证了糖尿病性血脂异常损害血管平滑肌Ca2+调节蛋白，特别是Na+/Ca2+交换器（NCX）的假设。我们进一步假设，耐力运动训练计划可以逆转或预防这种糖尿病引起的损害。将雄性尤卡坦猪随机分为4组：对照组(C)、脂肪组(F)、糖尿病高脂肪组（DF）和跑步机训练高脂肪组（DFX）。F、DF和DFX动物喂食致动脉粥样硬化的高热量饮食（2%的卡路里来自胆固醇），这使脂肪提供的卡路里百分比从8-46%增加，并刺激体重增加3倍于C动物。长期升高的血糖水平（300- 400mg /dL）在DF和DFX组维持了20周。DFX在65-75% HRmax下每周锻炼4天，每天30分钟，持续16周。牺牲后24小时内右冠状动脉平滑肌细胞分散，采用比值法（340/380）fura-2数字成像测量肌浆[Ca2+]（Cam）。该方案旨在检查NCX， sarco/内质网CaATPase （SERCA）和质乳CaATPase （PMCA）在缓冲去极化诱导的Ca2+进入和随后积累的Cam变化中的贡献。80 mM KCl （80K）对细胞去极化，诱导Ca2+内流，增加Cam。凸轮的变化是用响应曲线下的面积来确定的
Calcium (Ca2+) regulation in vascular smooth muscle cells is tightly controlled at the membrane level by channels, pumps, and exchangers. Any perturbation in the function or number of these Ca2+ regulatory mechanisms could potentially alter the balance between influx and efflux, ultimately resulting in overload of Ca2+ stores or elevated cytosolic or nuclear Ca2+. Both diabetes1, 2 and exercise3 independently have been shown to alter components of vascular smooth muscle Ca2+ regulation. We tested the hypothesis that diabetic dyslipidemia impairs vascular smooth muscle Ca2+ regulatory proteins, specifically the Na+/Ca2+ exchanger (NCX), in the Yucatan miniature swine model. We further hypothesized that a program of endurance exercise training would reverse or prevent this diabetes-induced impairment. Male Yucatan swine were randomly assigned to 4 groups: control (C), fat (F), diabetic high fat (DF), or treadmill-trained DF (DFX). F, DF, and DFX animals were fed an atherogenic, hypercaloric diet (2% of calories from cholesterol), which increased the% kcal provided from fat from 8-46% and stimulated weight gain 3-fold above C animals. Chronically elevated blood glucose levels (300-400 mg/dL) were maintained in DF and DFX for 20 weeks. DFX were exercised 4 days/week, 30 minutes/day at 65-75% HRmax for 16 weeks. Smooth muscle cells were dispersed from the right coronary artery within 24 hours after sacrifice, and myoplasmic [Ca2+](Cam) was measured by ratiometric (340/380) fura-2 digital imaging. 1 The protocol was designed to examine the contribution of the NCX, sarco/endoplasmic reticulum CaATPase (SERCA), and the plasmalemmal CaATPase (PMCA) in buffering depolarization-induced Ca2+ entry and subsequent changes in accumulated Cam. Cells were depolarized with 80 mM KCl (80K) to induce Ca2+ influx and increase Cam. Changes in Cam were determined using the area under the curve obtained in response