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首页> 外文期刊>Journal of Trace Elements in Experimental Medicine >Glutathione in Overweight Patients With Poorly Controlled Type 2 Diabetes
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Glutathione in Overweight Patients With Poorly Controlled Type 2 Diabetes

机译：谷胱甘肽对2型糖尿病控制不佳的超重患者

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摘要

Increased lipid peroxidation due to an altered intracellular ratio between free radicals and antioxidant systems has been associated with development of diabetic complications. This report explores the biochemical reliability of this hypothesis by measuring glutathione (GSH) in overweight patients with poorly controlled type 2 diabetes. GSH, a crucial antioxidant and cofactor for the selenium-dependent glutathione peroxidase (GSHPx), was analyzed in red blood cells. Ten overweight and poorly controlled type 2 diabetic patients (6 women and 4 men, age 45 -60 years, body mass index (BMI) 26 -32 kg/m~2, HbAlc > 9.4%) and 13 healthy normal weight controls (7 women and 6 men, age 40-60 years, BMI 20-2.5 kg/ m2, HbAlc <6,0 %) were included in the study. The intracellular level of GSH in red blood cells (mean 1.54 mmol/1) of the diabetic patients was reduced to 60% of reference values (mean 2-6 mmol/1). Reduced activity of GSHPx and increased levels of peroxides in diabetic patients have been found previously. Discussed are several mechanisms that contribute to the depletion of GSH in poorly controlled type 2 diabetic patients, involving reduced levels of NADPH that is essential for the regeneration of GSH in vivo, The probability of direct trapping of GSH to sugar aldehydes that invade the intracellular space in diabetic states should also be taken into account. Therapeutic trials with antioxi-dants that can regenerate the intracellular level of GSH are scarce but promising. An attractive hypothesis is that intracellular excesses of glucose inhibit the antioxidant systems primarily by its ability to cause depletion of the crucial protector GSH. The ultimate effects of such derangement of the protective systems against free radicals may involve vascular and neurological complications,
机译：由于自由基和抗氧化剂系统之间的细胞内比率改变而引起的脂质过氧化增加与糖尿病并发症的发展有关。本报告通过测量体重不足的2型糖尿病患者中的谷胱甘肽（GSH），探讨了该假设的生物化学可靠性。 GSH是硒依赖性谷胱甘肽过氧化物酶（GSHPx）的重要抗氧化剂和辅助因子，已在红细胞中进行了分析。 10名超重且控制不佳的2型糖尿病患者（6名女性和4名男性，年龄45 -60岁，体重指数（BMI）26 -32 kg / m〜2，HbAlc> 9.4％）和13名健康正常体重对照（7女性和6名男性，年龄40-60岁，BMI 20-2.5 kg / m2，HbAlc <6.0％）纳入研究。糖尿病患者红细胞的细胞内GSH水平（平均1.54 mmol / 1）降至参考值（平均2-6 mmol / 1）的60％。先前已经发现糖尿病患者中GSHPx的活性降低和过氧化物水平升高。讨论了几种控制不良的2型糖尿病患者中GSH耗竭的机制，包括降低NADPH的水平，这对于体内GSH的再生必不可少。直接将GSH捕获到糖醛中并侵入细胞内空间的可能性在糖尿病状态下也应予以考虑。可以再生细胞内GSH水平的抗氧化剂的治疗性试验很少，但是很有希望。一个有吸引力的假设是，细胞内过量的葡萄糖主要通过其导致关键保护因子GSH耗尽的能力抑制抗氧化系统。自由基保护系统的这种失调的最终结果可能涉及血管和神经系统并发症，

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