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补锌对链脲佐菌素诱导糖尿病大鼠受损小肠健康的改善作用。

Ameliorative effect of zinc supplementation on compromised small intestinal health in streptozotocin-induced diabetic rats.

机构信息

Department of Biochemistry, CSIR - Central Food Technological Research Institute, Mysore, 570 020, India.

Department of Biochemistry, CSIR - Central Food Technological Research Institute, Mysore, 570 020, India.

出版信息

Chem Biol Interact. 2019 Jul 1;307:37-50. doi: 10.1016/j.cbi.2019.04.018. Epub 2019 Apr 19.

DOI:10.1016/j.cbi.2019.04.018
PMID:31009641
Abstract

Zinc depletion during diabetes postulates a role for zinc nutrition in the management of associated complications. The present study evaluated zinc supplementation for countering the compromised intestinal integrity through moderation of oxidative stress and suppression of stress-stimulated inflammatory proliferation in streptozotocin-induced diabetic rats. Diabetic rats were provided with supplemental zinc for six weeks (5 and 10-times of normal level). Supplemental zinc nurtured diabetic groups evidenced a significant reversal of the disruption of intestinal ultra structure. While the brush border membrane (BBM) of diabetic animals showed decreased fluidity with increased cholesterol: phospholipid ratio and altered polyunsaturated to saturated fatty acid ratio, the same was countered in zinc supplementation. A stimulated activity of BBM-bound enzymes suggested a modulation in membrane dynamics in diabetic condition which was moderated in zinc treatment. Higher expression of the lipid oxidative markers, oxidative stress markers, concomitant inflammatory markers, cytokines, fibrosis factors and apoptotic regulatory proteins in the intestines were curbed by zinc supplementation. The pathological aberrations of the intestinal architecture in diabetic animals were similarly reverted. Thus, supplemental zinc has a favourable consequence in restricting the compromised intestinal health in diabetes which was exerted through a defensive stimulus on oxidative stress induced cytokines, inflammatory propagation, and subsequent injury.

摘要

糖尿病过程中的锌耗竭提示锌营养在管理相关并发症中的作用。本研究评估了锌补充剂通过调节氧化应激和抑制链脲佐菌素诱导的糖尿病大鼠应激刺激的炎症增殖来对抗受损的肠道完整性的作用。糖尿病大鼠补充锌 6 周(正常水平的 5 倍和 10 倍)。锌补充剂使糖尿病组的肠道超微结构破坏得到显著逆转。糖尿病动物的刷状缘膜(BBM)表现出流动性降低,胆固醇:磷脂比增加,多不饱和脂肪酸与饱和脂肪酸的比例改变,而在锌补充剂中则得到了逆转。BBM 结合酶的活性增加表明在糖尿病条件下膜动力学发生了调节,而在锌处理中则得到了缓和。锌补充剂抑制了肠道中脂质氧化标志物、氧化应激标志物、伴随的炎症标志物、细胞因子、纤维化因子和凋亡调节蛋白的更高表达。糖尿病动物的肠道结构的病理异常也得到了类似的逆转。因此,锌补充剂在限制糖尿病中受损的肠道健康方面具有有利的影响,这是通过对氧化应激诱导的细胞因子、炎症传播和随后的损伤产生防御性刺激来实现的。

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