Department of Physiology, Medical College, Dalian University, Dalian, China.
Hypertens Res. 2011 Dec;34(12):1239-45. doi: 10.1038/hr.2011.133. Epub 2011 Aug 4.
The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.
代谢综合征是 2 型糖尿病和心血管疾病的主要危险因素，是一系列代谢异常的综合征，包括肥胖、胰岛素抵抗、高血压和血脂异常。尽管系统性氧化应激和异常甲基化状态在代谢综合征的发生发展中具有重要作用，但它们的发生机制尚不清楚。消耗甲基的化合物的代谢会产生活性氧和消耗不稳定的甲基基团；因此，体内消耗甲基的化合物水平的慢性增加不仅会诱导氧化应激和随后的组织损伤，还会导致甲基池耗竭和随后的异常甲基化状态。在过去几十年中，由于污染、食品添加剂、烟酸强化和高肉消费，消耗甲基的化合物的摄入量大大增加。因此，增加的甲基供体可能在代谢综合征及其相关疾病的发生和流行中起因果作用。此外，减少消耗甲基的化合物和其他外源性化合物的消除/代谢的因素（例如，汗腺不活跃和肝功能下降）或增加内源性消耗甲基的化合物的生成（例如，精神压力引起的儿茶酚胺释放增加），可能会加速代谢综合征的进展。基于当前的营养知识以及代谢综合征及其相关疾病的流行病学、生态学、临床和实验室研究的现有证据，本文综述了甲基供应-消耗失衡与代谢综合征之间的关系，并提出了代谢综合征及其相关疾病发病机制和流行的新机制。
