Diabetes Research Group, College of Medicine, Swansea University, Singleton Park, Swansea, UK.
Diabetes Research Group, College of Medicine, Swansea University, Singleton Park, Swansea, UK.
Diabetes Res Clin Pract. 2014 Dec;106(3):627-33. doi: 10.1016/j.diabres.2014.09.054. Epub 2014 Oct 25.
In the past 30 years, prevalence of obesity has almost trebled resulting in an increased incidence of type 2 diabetes mellitus and other co-morbidities. Visceral adipose tissue is believed to play a vital role, but underlying mechanisms remain unclear. Our aim was to investigate changes in markers of oxidative damage in human visceral adipose tissue to determine levels of oxidative burden that may be attributed to obesity and/or diabetes.
Visceral adipose tissue samples from 61 subjects undergoing abdominal surgery grouped as lean, obese and obese with type 2 diabetes mellitus, were examined using 3 different markers of oxidative stress. Malondialdehyde (MDA) concentration was measured as a marker of lipid peroxidation, telomere length and Comet assay as markers of oxidative DNA damage.
No significant difference in MDA concentration, telomere length and DNA damage was observed between groups, although longer telomere lengths were seen in the obese with diabetes group compared to the obese group (P<0.05). Lower MDA concentration and longer telomere length were seen in subjects with diabetes compared to those without (P<0.05). DNA damage, analysed via Comet assay, was significantly lower in subjects with diabetes compared to those without (P<0.05).
A paradoxical decrease in oxidative stress and DNA damage was observed in samples from subjects with type 2 diabetes mellitus. Further work is required to investigate this further, however this phenomenon may be due to an up regulation of antioxidant defences in adipose tissue.
在过去的 30 年中，肥胖的患病率几乎增加了两倍，导致 2 型糖尿病和其他合并症的发病率上升。内脏脂肪组织被认为起着至关重要的作用，但潜在的机制仍不清楚。我们的目的是研究人体内脏脂肪组织中氧化损伤标志物的变化，以确定可能归因于肥胖和/或糖尿病的氧化应激水平。
对 61 名接受腹部手术的患者的内脏脂肪组织样本进行研究，这些患者分为瘦、肥胖和肥胖合并 2 型糖尿病。使用 3 种不同的氧化应激标志物来检测氧化损伤。丙二醛（MDA）浓度作为脂质过氧化的标志物进行测量，端粒长度和彗星试验作为氧化 DNA 损伤的标志物。
尽管糖尿病肥胖组的端粒长度长于肥胖组（P<0.05），但各组之间 MDA 浓度、端粒长度和 DNA 损伤无显著差异。与无糖尿病者相比，糖尿病患者的 MDA 浓度较低，端粒长度较长（P<0.05）。与无糖尿病者相比，糖尿病患者的 Comet 试验分析的 DNA 损伤明显较低（P<0.05）。
在 2 型糖尿病患者的样本中观察到氧化应激和 DNA 损伤的反常性降低。需要进一步研究这一现象，但这种现象可能是由于脂肪组织中抗氧化防御的上调。
