Ca2+ is implicated in the aetiology of many diseases including diabetes but there are few studies on the mechanism(s) of the altered Ca2+ regulation. Using human lymphocytes, we studied cytosolic calcium (Cai) and various Ca2+ transport mechanisms in subjects with Type 2 diabetes mellitus and control subjects. Ca2+-specific fluorescent probes (Fura-2 and Fluo-3) were used to monitor the Ca2+ signals. Thapsigargin, a potent and specific inhibitor of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA), was used to study Ca2+- store dependent Ca2+ fluxes. Significant (P < 0.05) elevation of basal Cai levels was observed in lymphocytes from diabetic subjects. Cai levels were positively correlated with fasting, plasma glucose and HbAlc. There was also a significant (P < 0.05) reduction in plasma membrane calcium (PMCA) ATPase activity in diabetic subjects compared to controls. Cells from Type 2 diabetics exhibited an increased Ca2+ influx (as measured both by Fluo-3 fliorescence and C45a assays) as a consequence of of thapsigargin-mediated Ca2+ store depletion. Upon addition of Mn2+ (a surrogate of Ca2+), the fura-2 fluorescence decayed in an exponential fashion and the rate and extent of this decline was steeper and greater in cells from type 2 diabetic patients. There was also a significant (P < 0.05) difference in the Na+/Ca2+ exchange activity in Type 2 diabetic patients, both under resting conditions and after challenging the cells with thapsigargin, when the internal store Ca2+ sequestration was circumvented. Pharmacological activation of protein kinase C (PKC) in cells from patients resulted in only partial inhibition of Ca2+ entry. We conclude that cellular Ca2+ accumulation in cells from Type 2 diabetes results from (a) reduction in PMCA ATPase activity, (b) modulation of Na+/Ca2+ exchange and (3) increased Ca2+ influx across the plasma membrane."> 机械的证据改变Ca2 +内稳态的2型糖尿病 - raybet雷竞app,雷竞技官网下载,雷电竞下载苹果

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体积 1 |文章的ID 304074年 | https://doi.org/10.1155/EDR.2000.275

Muthuswamy Balasubramanyam Ramalingham a,巴拉Balakrishnan Subashini Viswanathan汉, ”机械的改变的证据 Ca 2 + 在2型糖尿病体内平衡”,糖尿病研究期刊》的研究, 卷。1, 文章的ID304074年, 13 页面, 2000年。 https://doi.org/10.1155/EDR.2000.275

机械的改变的证据 Ca 2 + 在2型糖尿病体内平衡

Muthuswamy Balasubramanyam,^1,3 Ramalingham a巴拉,¹ Balakrishnan Subashini,¹ 和 Viswanathan汉²

¹安娜大学生物技术中心,钦奈600025年,印度

²马德拉斯糖尿病研究基金会,Gopalapuram钦奈600086年,印度

³马德拉斯糖尿病研究基金会(MDRF), 35岁的史密斯•康兰,Gopalapuram,钦奈600086年,印度

收到了 1999年11月08

接受 2000年6月17日

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改变胞质 Ca 2 + 涉及病因学的很多疾病,包括糖尿病,而很少有研究机制(s)的改变 Ca 2 + 监管。用人类淋巴细胞,我们研究了胞质钙( Ca 我 )和各种 Ca 2 + 与2型糖尿病受试者的传输机制和控制对象。 Ca 2 + 特殊技能荧光探针(Fura-2和Fluo-3)被用来监控 Ca 2 + 信号。Thapsigargin,石棺的有力和特定抑制剂(endo)血浆的网 Ca 2 + 腺苷三磷酸酶(SERCA的),是用于研究 Ca 2 + ——存储的依赖 Ca 2 + 通量。重要的(P< 0.05)基底高程 Ca 我在淋巴细胞水平观察糖尿病主题。 Ca 我与空腹水平呈正相关,血浆葡萄糖和HbAlc。还有一个重要的(P< 0.05)降低质膜钙(PMCA)腺苷三磷酸酶活动相比,糖尿病患者控制。细胞的2型糖尿病患者表现出增加 Ca 2 + 涌入(通过衡量Fluo-3 fliorescence和 C 45 一个 thapsigargin-mediated化验)的结果 Ca 2 + 存储损耗。在添加锰 2 + (代理 Ca 2 + 以指数方式),fura-2荧光衰变的速率和程度跌幅和更大的2型糖尿病患者的细胞。还有一个重要的(P< 0.05)差异 Na + / Ca 2 + 交换活动在2型糖尿病患者,在静止条件下和与thapsigargin挑战细胞后,当内部存储 Ca 2 + 封存被规避。药理激活的蛋白激酶C (PKC)在细胞患者导致只有部分抑制 Ca 2 + 条目。我们得出这样的结论:细胞 Ca 2 + 积累在细胞(a)减少2型糖尿病结果PMCA atp酶活动,(b)调制的 Na + / Ca 2 + 交换和(3)增加 Ca 2 + 质膜流入。

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