肿瘤坏死因子α对肥胖和糖尿病患者缺血后调节结果的影响。

Experimental Diabetes Research Pub Date : 2012-01-01 Epub Date: 2012-10-17 DOI:10.1155/2012/502654
Lydia Lacerda, Lionel H Opie, Sandrine Lecour
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引用次数: 0

摘要

肥胖和糖尿病会导致心血管疾病,并改变细胞因子谱。细胞因子肿瘤坏死因子α(TNFα)可在缺血后调节(IPostC)过程中激活保护性信号级联。然而,大多数成功的缺血后调节临床研究都不包括肥胖和/或糖尿病患者。我们的目的是研究 TNFα 对肥胖或糖尿病小鼠 IPostC 结果的影响。用高碳水化合物饮食(HCD)喂养TNF基因敲除或野生型小鼠11周,以诱导小鼠中度肥胖。另一组小鼠通过腹腔注射链脲佐菌素诱发糖尿病。然后分离心脏并对其进行缺血(整体缺血 35 分钟)和 45 分钟再灌注。HCD 增加了体重、血浆胰岛素和瘦素水平,而血糖水平保持不变。在链脲佐菌素处理的小鼠中,血糖、血浆瘦素和胰岛素都发生了变化。在对照组、肥胖或糖尿病小鼠中,IpostC 对正常动物具有保护作用。在 TNF 基因敲除小鼠中,IPostC 未能保护对照组和糖尿病小鼠的心脏,而在肥胖小鼠的心脏中则观察到轻微的保护作用。我们的数据证实了TNFα与并发症严重程度相关的双向作用,并表明糖尿病和/或轻度肥胖患者仍可从IPostC中获益。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Influence of tumour necrosis factor alpha on the outcome of ischaemic postconditioning in the presence of obesity and diabetes.

Influence of tumour necrosis factor alpha on the outcome of ischaemic postconditioning in the presence of obesity and diabetes.

Influence of tumour necrosis factor alpha on the outcome of ischaemic postconditioning in the presence of obesity and diabetes.

Influence of tumour necrosis factor alpha on the outcome of ischaemic postconditioning in the presence of obesity and diabetes.

Obesity and diabetes contribute to cardiovascular disease and alter cytokine profile. The cytokine, tumour necrosis factor alpha (TNFα), activates a protective signalling cascade during ischaemic postconditioning (IPostC). However, most successful clinical studies with IPostC have not included obese and/or diabetic patients. We aimed to investigate the influence of TNFα on the outcome of IPostC in obese or diabetic mice. TNF knockout or wildtype mice were fed for 11 weeks with a high carbohydrate diet (HCD) to induce modest obesity. Diabetes was induced in a separate group by administration of a single intraperitoneal injection of streptozotocin. Hearts were then isolated and subjected to ischaemia (35 min of global ischaemia) followed by 45 min of reperfusion. HCD increased body weight, plasma insulin and leptin levels while the glucose level was unchanged. In streptozotocin-treated mice, blood glucose, plasma leptin and insulin were altered. Control, obese or diabetic mice were protected with IPostC in wiltype animals. In TNF knockout mice, IPostC failed to protect control and diabetic hearts while a slight protection was observed in obese hearts. Our data confirm a bidirectional role for TNFα associated with the severity of concomitant comorbidities and suggest that diabetic and/or modestly obese patients may still benefit from IPostC.

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来源期刊
Experimental Diabetes Research
Experimental Diabetes Research 医学-内分泌学与代谢
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