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Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models
Author(s) -
Meneses Maria E.,
Camargo Antonio,
PerezMartinez Pablo,
DelgadoLista Javier,
CruzTeno Cristina,
JimenezGomez Yolanda,
Paniagua Juan A.,
GutierrezMariscal Francisco M.,
Tinahones Francisco J.,
VidalPuig Antonio,
Roche Helen M.,
PerezJimenez Francisco,
Malagon Maria M.,
LopezMiranda Jose
Publication year - 2011
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201100200
Subject(s) - postprandial , adipose tissue , medicine , endocrinology , polyunsaturated fatty acid , metabolic syndrome , fatty acid , obesity , biology , biochemistry , insulin
Scope: Dysfunctional adipose tissue may be an important trigger of molecular inflammatory pathways that cause cardiovascular diseases. Our aim was to determine whether the specific quality and quantity of dietary fat produce differential postprandial inflammatory responses in adipose tissue from metabolic syndrome (MetS) patients. Methods and results: A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to 1 of 4 diets: (i) high‐saturated fatty acid (HSFA), (ii) high‐monounsaturated fatty acid (HMUFA), (iii) low‐fat, high‐complex carbohydrate diet supplemented with n −3 polyunsaturated fatty acids (PUFA) (LFHCC n −3), and (iv) low‐fat, high‐complex carbohydrate diet supplemented with placebo (LFHCC), for 12 wk each. A fat challenge reflecting the fatty acid composition as the original diets was conducted post‐intervention. We found that p65 gene expression is induced in adipose tissue ( p =0.003) at the postprandial state. In addition, IκBα ( p <0.001), MCP‐1 ( p <0.001) and IL‐1β ( p <0.001) gene expression was equally induced in the postprandial state, regardless of the quality and quantity of the dietary fat. Notably, IL‐6 transcripts were only detected in the postprandial state. Conclusions: Our results indicate that individuals with MetS typically exhibit exacerbated adipose tissue postprandial inflammatory responses, which seem to be independent of the quality and quantity of dietary fat.