Department of Biochemistry and Nutrition, CSIR-Central Food Technological Research Institute, Mysore, 570 020, India.
Department of Biochemistry and Nutrition, CSIR-Central Food Technological Research Institute, Mysore, 570 020, India.
J Nutr Biochem. 2018 Apr;54:113-129. doi: 10.1016/j.jnutbio.2017.11.008. Epub 2017 Dec 11.
Zinc deficiency during diabetes projects a role for zinc nutrition in the management of diabetic nephropathy. The current study explored whether zinc supplementation protects against diabetic nephropathy through modulation of kidney oxidative stress and stress-induced expression related to the inflammatory process in streptozotocin-induced diabetic rats. Groups of hyperglycemic rats were exposed to dietary interventions for 6 weeks with zinc supplementation (5 times and 10 times the normal level). Supplemental-zinc-fed diabetic groups showed a significant reversal of increased kidney weight and creatinine clearance. There was a significant reduction in hyperlipidemic condition along with improved PUFA:SFA ratio in the renal tissue. Expression of the lipid oxidative marker and expression of inflammatory markers, cytokines, fibrosis factors and apoptotic regulatory proteins observed in diabetic kidney were beneficially modulated by zinc supplementation, the ameliorative effect being concomitant with elevated antiapoptosis. There was a significant reduction in advanced glycation, expression of the receptor of the glycated products and oxidative stress markers. Zinc supplementation countered the higher activity and expression of polyol pathway enzymes in the kidney. Overexpression of the glucose transporters, as an adaptation to the increased need for glucose transport in diabetic condition, was minimized by zinc treatment. The pathological abnormalities in the renal architecture of diabetic animals were corrected by zinc intervention. Thus, dietary zinc supplementation has a significant beneficial effect in the control of diabetic nephropathy. This was exerted through a protective influence on oxidative-stress-induced cytokines, inflammatory proliferation and consequent renal injury.
锌缺乏症在糖尿病中的作用表明锌营养在糖尿病肾病的治疗中有一定作用。本研究探讨了锌补充是否通过调节肾脏氧化应激和应激诱导的与炎症过程相关的表达来预防糖尿病肾病，该研究在链脲佐菌素诱导的糖尿病大鼠中进行。高血糖大鼠组接受了 6 周的饮食干预，其中包括锌补充（正常水平的 5 倍和 10 倍）。补充锌的糖尿病组大鼠的肾脏重量和肌酐清除率显著降低。肾脏组织中的血脂异常情况显著改善，同时多不饱和脂肪酸与饱和脂肪酸的比例也得到了提高。糖尿病肾脏中观察到的脂质氧化标志物的表达和炎症标志物、细胞因子、纤维化因子和凋亡调节蛋白的表达均得到了锌补充的有益调节，这种改善作用伴随着抗凋亡作用的增强。晚期糖基化产物的表达、糖基化产物受体和氧化应激标志物的表达也显著降低。锌补充可抑制肾脏中多元醇途径酶的更高活性和表达。高血糖条件下对葡萄糖转运的需求增加，导致葡萄糖转运体的过度表达，而锌处理可减少这种过度表达。锌干预纠正了糖尿病动物肾脏结构的病理异常。因此，膳食锌补充对控制糖尿病肾病有显著的有益作用。这种作用是通过对氧化应激诱导的细胞因子、炎症增殖和随后的肾脏损伤产生保护作用来实现的。
