Fatty acids, epigenetic mechanisms and chronic diseases: a systematic review.
Lipids Health Dis
; 18(1): 178, 2019 Oct 15.
Article
em En
| MEDLINE
| ID: mdl-31615571
BACKGROUND: Chronic illnesses like obesity, type 2 diabetes (T2D) and cardiovascular diseases, are worldwide major causes of morbidity and mortality. These pathological conditions involve interactions between environmental, genetic, and epigenetic factors. Recent advances in nutriepigenomics are contributing to clarify the role of some nutritional factors, including dietary fatty acids in gene expression regulation. This systematic review assesses currently available information concerning the role of the different fatty acids on epigenetic mechanisms that affect the development of chronic diseases or induce protective effects on metabolic alterations. METHODS: A targeted search was conducted in the PubMed/Medline databases using the keywords "fatty acids and epigenetic". The data were analyzed according to the PRISMA-P guidelines. RESULTS: Consumption fatty acids like n-3 PUFA: EPA and DHA, and MUFA: oleic and palmitoleic acid was associated with an improvement of metabolic alterations. On the other hand, fatty acids that have been associated with the presence or development of obesity, T2D, pro-inflammatory profile, atherosclerosis and IR were n-6 PUFA, saturated fatty acids (stearic and palmitic), and trans fatty acids (elaidic), have been also linked with epigenetic changes. CONCLUSIONS: Fatty acids can regulate gene expression by modifying epigenetic mechanisms and consequently result in positive or negative impacts on metabolic outcomes.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Gorduras na Dieta
/
Doenças Cardiovasculares
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Epigênese Genética
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Diabetes Mellitus Tipo 2
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Metabolismo dos Lipídeos
/
Obesidade
Tipo de estudo:
Prognostic_studies
/
Systematic_reviews
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Lipids Health Dis
Assunto da revista:
BIOQUIMICA
/
METABOLISMO
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
México
País de publicação:
Reino Unido