title: Postprandial inflammatory response in adipose tissue of patients with metabolic syndrome after the intake of different dietary models.
abstract: METHODS
  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.
  
  
  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.
authors.affiliation: Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Cordoba, Spain.
authors.forename: Maria E
authors.initials: ME
authors.lastname: Meneses
authors.forename: Antonio
authors.initials: A
authors.lastname: Camargo
authors.forename: Pablo
authors.initials: P
authors.lastname: Perez-Martinez
authors.forename: Javier
authors.initials: J
authors.lastname: Delgado-Lista
authors.forename: Cristina
authors.initials: C
authors.lastname: Cruz-Teno
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Jimenez-Gomez
authors.forename: Juan A
authors.initials: JA
authors.lastname: Paniagua
authors.forename: Francisco M
authors.initials: FM
authors.lastname: Gutierrez-Mariscal
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Tinahones
authors.forename: Antonio
authors.initials: A
authors.lastname: Vidal-Puig
authors.forename: Helen M
authors.initials: HM
authors.lastname: Roche
authors.forename: Francisco
authors.initials: F
authors.lastname: Perez-Jimenez
authors.forename: Maria M
authors.initials: MM
authors.lastname: Malagon
authors.forename: Jose
authors.initials: J
authors.lastname: Lopez-Miranda
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D004032:Diet; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage*; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D020672:I-kappa B Proteins / Q000235:genetics / Q000378:metabolism; D007249:Inflammation / Q000503:physiopathology*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology*; D008875:Middle Aged; D000072000:NF-KappaB Inhibitor alpha; D019518:Postprandial Period / Q000187:drug effects*
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D005229:Fatty Acids, Monounsaturated; D015525:Fatty Acids, Omega-3; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D015850:Interleukin-6; C000606204:NFKBIA protein, human; D000072000:NF-KappaB Inhibitor alpha