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Mitochondria-Based Model for Fetal Origin of Adult Disease and Insulin Resistance

机译：基于线粒体的成人疾病和胰岛素抵抗的胎儿胎儿模型

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Insulin resistance has been recognized as the fundamental underlying metabolic defect in the pathogenesis of metabolic syndrome, a clustering of cardiovascular risk factors such as diabetes, hypertension, dyslipidemia, and obesity. Recent studies established that mitochondrial dysfunction is involved in insulin resistance in general and fetal origin of this state in particular. Because genes are the fundamental molecular basis of inheritance—and thus the cornerstones of evolution—a model explaining insulin resistance is based at the gene level at best. Since a certain mtDNA polymorphism, 16189T>C, is associated with insulin resistance, mtDNA has to be a basic component of the gene-based model. We developed a mitochondria-based model that explains insulin resistance in terms of quantitative and qualitative change of the mitochondrion and its DNA. This model can accommodate several important hypotheses, such as thrifty genotype hypothesis, thrifty phenotype hypothesis, fetal insulin hypothesis, contribution of metabolic imprinting by epigenetic changes, and many other features associated with insulin resistance. We will discuss mechanisms that indicate why the perturbed initial condition of mitochondrial function should lead to the reduced insulin sensitivity.
机译：胰岛素抵抗已被确认为在代谢综合症的发病机理的基本潜在代谢缺陷，心血管风险聚类因素，如糖尿病，高血压，血脂异常和肥胖。最近的研究证实，线粒体功能障碍参与胰岛素抵抗，尤其在该状态下的一般和胎儿起源。因为基因的基本分子基础继承的，因此演进一个模型解释胰岛素抵抗的基石是基于在充其量基因水平。由于在一定的mtDNA多态性，16189T> C，与胰岛素抗性相关，线粒体DNA必须是基于基因的模型的一个基本组成部分。我们开发了一个基于线粒体模型，解释了线粒体和DNA的定量和定性的变化而言胰岛素抵抗。该模型可以容纳几个重要的假设，诸如节俭基因型假设，节俭表型假说，胎儿胰岛素假说，通过表观遗传改变的代谢印迹的贡献，并与胰岛素抵抗有关许多其他功能。我们将讨论说明为什么线粒体功能的扰动初始条件应该导致胰岛素敏感性降低的机制。

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