Polymorphism at the TNF ‐alpha gene interacts with M editerranean diet to influence triglyceride metabolism and inflammation status in metabolic syndrome patients: F rom the CORDIOPREV clinical trial
2014; Wiley; Volume: 58; Issue: 7 Linguagem: Inglês
10.1002/mnfr.201300723
ISSN1613-4133
AutoresFrancisco Gómez-Delgado, Juan F. Alcalá‐Díaz, Antonio García‐Ríos, Javier Delgado‐Lista, Ana M. Ortiz-Morales, Oriol Alberto Rangel-Zúñiga, Francisco J. Tinahones, Lorena González-Guardia, Marı́a M. Malagón, Enrique Bellido‐Muñoz, José M. Ordovás, Francisco Pérez‐Jiménez, José López‐Miranda, Pablo Pérez‐Martínez,
Tópico(s)Adipose Tissue and Metabolism
ResumoScope To examine whether the consumption of a M editerranean diet ( M ed D iet), compared with a low‐fat diet, interacts with two single nucleotide polymorphisms at the tumor necrosis factor alpha gene (rs1800629, rs1799964) in order to improve triglycerides ( TG ), glycemic control, and inflammation markers. Methods and results Genotyping, biochemical measurements, dietary intervention, and oral fat load test meal were determined in 507 metabolic syndrome ( M et S ) patients selected from all the subjects included in CORDIOPREV clinical trial ( n = 1002). At baseline, G / G subjects ( n = 408) at the rs1800629 polymorphism, showed higher fasting and postprandial TG ( p = 0.003 and p = 0.025, respectively), and high sensitivity C ‐reactive protein (hsCRP) ( p = 0.003) plasma concentrations than carriers of the minor A ‐allele ( G / A + A / A ) ( n = 99). After 12 months of M ed D iet, baseline differences between genotypes disappeared. The decrease in TG and hsCRP was statistically significant in G/G subjects ( n = 203) compared with carriers of the minor A ‐allele ( p = 0.005 and p = 0.034, respectively) ( n = 48). No other gene–diet interactions were observed in either diet. Conclusion These results suggest that the rs1800629 at the tumor necrosis factor alpha gene interacts with M ed D iet to influence TG metabolism and inflammation status in M et S subjects. Understanding the role of gene–diet interactions may be the best strategy for personalized treatment of M et S .
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