Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models
✍ Scribed by Maria E. Meneses; Antonio Camargo; Pablo Perez-Martinez; Javier Delgado-Lista; Cristina Cruz-Teno; Yolanda Jimenez-Gomez; Juan A. Paniagua; Francisco M. Gutierrez-Mariscal; Francisco J. Tinahones; Antonio Vidal-Puig; Helen M. Roche; Francisco Perez-Jimenez; Maria M. Malagon; Jose Lopez-Miranda
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 235 KB
- Volume
- 55
- Category
- Article
- ISSN
- 1613-4125
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✦ Synopsis
Abstract
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.