Roche Helen M, Phillips Catherine, Gibney Michael J
Nutrigenomics Research Group, Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin, Dublin 8, Republic of Ireland.
Proc Nutr Soc. 2005 Aug;64(3):371-7. doi: 10.1079/pns2005445.
The metabolic syndrome is a very common disease associated with an increased risk of type 2 diabetes mellitus (T2DM) and CVD. The clinical characteristics of the metabolic syndrome include insulin resistance, dyslipidaemia, abdominal obesity and hypertension. The diverse clinical characteristics illustrate the complexity of the disease process, which involves several dysregulated metabolic pathways. Thus, multiple genetic targets must be involved in the pathogenesis and progression of the metabolic syndrome. Nevertheless, the human genome has not changed markedly in the last decade but the prevalence of the metabolic syndrome has increased exponentially, which illustrates the importance of gene-environmental interactions. There is good evidence that nutrition plays an important role in the development and progression of the metabolic syndrome. Indeed, obesity is a key aetiological factor in the development of the metabolic syndrome. Understanding the biological impact of gene-nutrient interactions will provide a key insight into the pathogenesis and progression of diet-related polygenic disorders, including the metabolic syndrome. The present paper will explore the interactions between genetic background and dietary exposure or nutritional therapy, focusing on the role of dietary fatty acids within the context of nutrient regulation of gene expression and individual responsiveness to dietary therapy. Only with a full understanding of gene-gene, gene-nutrient and gene-nutrient-environment interactions can the molecular basis of the metabolic syndrome be solved to minimise the adverse health effects of obesity and reduce the risk of the metabolic syndrome, and subsequent T2DM and CVD.
代谢综合征是一种非常常见的疾病，与2型糖尿病（T2DM）和心血管疾病（CVD）风险增加相关。代谢综合征的临床特征包括胰岛素抵抗、血脂异常、腹型肥胖和高血压。这些多样的临床特征说明了疾病过程的复杂性，该过程涉及多个失调的代谢途径。因此，多个基因靶点必定参与了代谢综合征的发病机制和进展。然而，在过去十年中人类基因组并未发生显著变化，但代谢综合征的患病率却呈指数级增长，这说明了基因 - 环境相互作用的重要性。有充分证据表明，营养在代谢综合征的发生和发展中起重要作用。事实上，肥胖是代谢综合征发生的关键病因。了解基因 - 营养素相互作用的生物学影响将为深入了解包括代谢综合征在内的饮食相关多基因疾病的发病机制和进展提供关键线索。本文将探讨遗传背景与饮食暴露或营养治疗之间的相互作用，重点关注膳食脂肪酸在基因表达的营养调控以及个体对饮食治疗反应性方面的作用。只有充分理解基因 - 基因、基因 - 营养素和基因 - 营养素 - 环境之间的相互作用，才能解决代谢综合征的分子基础问题，以尽量减少肥胖对健康的不利影响，并降低代谢综合征以及后续T2DM和CVD的风险。
