Margaryan Sona, Witkowicz Agata, Partyka Anna, Yepiskoposyan Levon, Manukyan Gayane, Karabon Lidia
Laboratory of Molecular and Cellular Immunology, Institute of Molecular Biology, National Academy of Sciences, Yerevan, Armenia.
Laboratory of Immunopathology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
Postepy Hig Med Dosw (Online). 2017 Oct 19;71(0):895-900. doi: 10.5604/01.3001.0010.5386.
Type 2 diabetes mellitus (T2DM) and obesity are metabolic disorders whose major hallmark is insulin resistance. Impaired mitochondrial activity, such as reduced ratio of energy production to respiration, has been implicated in the development of insulin resistance. Uncoupling proteins (UCPs) are proton carriers, expressed in the mitochondrial inner membrane, that uncouple oxygen consumption by the respiratory chain from ATP synthesis.
The aim of the study was to determine transcriptional levels of UCP1 and UCP2 in peripheral blood mononuclear cells (PBMCs) from patients with metabolic disorders: T2DM, obesity and from healthy individuals.
MATERIAL/METHODS: The mRNA levels of UCP1, UCP2 were determined by Real-Time PCR method using Applied Biosystems assays.
The UCP1 mRNA expression level was not detectable in the majority of studied samples, while very low expression was found in PBMCs from 3 obese persons. UCP2 mRNA expression level was detectable in all samples. The median mRNA expression of UCP2 was lower in all patients with metabolic disorders as compared to the controls (0.20+0.14 vs. 0.010+0.009, p=0.05). When compared separately, the differences of medians UCP2 mRNA expression level between the obese individuals and the controls as well as between the T2DM patients and the controls did not reach statistical significance.
Decreased UCP2 gene expression in mononuclear cells from obese and diabetic patients might contribute to the immunological abnormalities in these metabolic disorders and suggests its role as a candidate gene in future studies of obesity and diabetes.
2型糖尿病（T2DM）和肥胖是代谢紊乱疾病，其主要特征是胰岛素抵抗。线粒体活性受损，如能量产生与呼吸的比率降低，与胰岛素抵抗的发生有关。解偶联蛋白（UCPs）是质子载体，在线粒体内膜表达，可使呼吸链的氧气消耗与ATP合成解偶联。
本研究旨在确定代谢紊乱患者（T2DM、肥胖症患者）及健康个体外周血单核细胞（PBMCs）中UCP1和UCP2的转录水平。
材料/方法：使用Applied Biosystems检测方法通过实时PCR法测定UCP1、UCP2的mRNA水平。
在大多数研究样本中未检测到UCP1 mRNA表达水平，而在3名肥胖者的PBMCs中发现极低的表达。所有样本中均可检测到UCP2 mRNA表达水平。与对照组相比，所有代谢紊乱患者中UCP2的mRNA表达中位数均较低（0.20 + 0.14对0.010 + 0.009，p = 0.05）。单独比较时，肥胖个体与对照组之间以及T2DM患者与对照组之间UCP2 mRNA表达水平中位数的差异未达到统计学意义。
肥胖和糖尿病患者单核细胞中UCP2基因表达降低可能导致这些代谢紊乱中的免疫异常，并提示其在未来肥胖和糖尿病研究中作为候选基因的作用。
