4.7 Review

Metabolic syndrome: Evidences for a personalized nutrition

期刊

MOLECULAR NUTRITION & FOOD RESEARCH
卷 56, 期 1, 页码 67-76

出版社

WILEY
DOI: 10.1002/mnfr.201100531

关键词

Diet; Gene-diet interaction; Metabolic syndrome; Nutrigenomics; Polymorphism

资金

  1. Spanish Ministry of Science and Innovation [AGL 2004-07907, AGL2006-01979, AGL2009-12270, SAF07-62005, FIS PI10/01041, PI10/02412]
  2. Consejeria de Economia, Innovacion y Ciencia, Proyectos de Investigacion de Excelencia, Junta de Andalucia [P06-CTS-01425, CTS5015, AGR922]
  3. Consejeria de Salud, Junta de Andalucia [06/128, 07/43, PI0193/09, 06/129, 0118/08, PI-0252/09, PI-0058/10]
  4. Fondo Europeo de Desarrollo Regional (FEDER)
  5. Centro de Excelencia Investigadora en Aceite de Oliva y Salud (CEAS)
  6. ISCIII

向作者/读者索取更多资源

Both insulin resistance and dyslipidaemia are determined by genetic and environmental factors. Depending on their expression and their function, gene variants may influence either insulin action or other metabolic traits. Nutrition also plays an important role in the development and progression of these conditions. Genetic background may interact with habitual dietary fat composition, affecting predisposition to insulin resistance syndrome and individual responsiveness to changes in dietary fat intake. In this context, nutrigenetics has emerged as a multidisciplinary field focusing on studying the interactions between nutritional and genetic factors and health outcomes. Due to the complex nature of geneenvironment interactions, however, dietary therapy may require a personalized nutrition approach in the future. Although the results have not always been consistent, gene variants that affect primary insulin action, and particularly their interaction with the environment, are important modulators of glucose metabolism. The purpose of this review is to present some evidence of studies that have already demonstrated the significance of genenutrient interactions (adiponectin gene, Calpain-10, glucokinase regulatory protein, transcription factor 7-like 2, leptin receptor, scavenger receptor class B type I etc.) that influence insulin resistance in subjects with metabolic syndrome.

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