Singh R, Hattersley A T, Harries L W
Institute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, UK.
Diabet Med. 2007 Jul;24(7):784-7. doi: 10.1111/j.1464-5491.2007.02164.x. Epub 2007 May 29.
Mitochondrial depletion in pancreatic beta cells is known to reduce glucose stimulated insulin secretion. We aimed to determine whether the offspring of patients with early onset Type 2 diabetes had reduced peripheral blood mitochondrial content relative to control subjects and whether this could lead to a predisposition to type 2 diabetes in later life.
We measured the levels of mitochondria relative to a single copy genomic target by real time polymerase chain reaction in a series of peripheral blood samples taken from the offspring of Caucasian patients with Type 2 diabetes and matched controls. Measures of insulin sensitivity and beta cell function were also taken.
In contrast with previous studies, mitochondrial DNA content was not decreased in the offspring of patients with Type 2 diabetes relative to matched controls in our cohort. Conversely, we noted a small proliferation in mitochondrial numbers in our case subjects. In agreement with these findings, no correlations with either insulin sensitivity or beta cell function were noted.
Our results indicate that reduced mitochondrial DNA content in peripheral blood is not a risk factor for the development of Type 2 diabetes in the offspring of patients with early onset Type 2 diabetes.
已知胰腺β细胞中的线粒体耗竭会降低葡萄糖刺激的胰岛素分泌。我们旨在确定早发型2型糖尿病患者的后代相对于对照受试者外周血线粒体含量是否降低，以及这是否会导致其在晚年易患2型糖尿病。
我们通过实时聚合酶链反应，在一系列取自白种人2型糖尿病患者后代及匹配对照的外周血样本中，测量相对于单拷贝基因组靶点的线粒体水平。同时还进行了胰岛素敏感性和β细胞功能的测量。
与之前的研究相反，在我们的队列中，2型糖尿病患者后代的线粒体DNA含量相对于匹配对照并未降低。相反，我们注意到病例组受试者的线粒体数量有少量增加。与这些发现一致，未观察到与胰岛素敏感性或β细胞功能的相关性。
我们的结果表明，外周血线粒体DNA含量降低并非早发型2型糖尿病患者后代发生2型糖尿病的危险因素。
