Dietary fat modifies the postprandial inflammatory state in subjects with metabolic syndrome: the LIPGENE study.
METHODS
Our aim was to investigate whether the inflammatory state associated to metabolic syndrome (MetS) patients is affected by diets with different fat quality and quantity.


RESULTS
Seventy-five subjects from LIPGENE cohort were included in this feeding trial and randomly assigned to one of four diets: high saturated fatty acids (HSFA); high monounsaturated fatty acids (HMUFA) and two low-fat, high complex carbohydrate (LFHCC) diets, supplemented with long-chain n-3 polyunsaturated fatty acids (LFHCC n-3) or placebo (LFHCC), for 12 weeks each. A postprandial fat challenge, reflecting the intervention dietary fat composition, was conducted post-intervention. The HMUFA diet significantly reduced postprandial nuclear transcription factor-kappaB (NF-kB) activity and the nuclear p65 protein levels relative to fasting values (p < 0.05). Furthermore, we observed a postprandial decrease in this protein with the HMUFA diet compared with the HSFA and LFHCC diets (p < 0.05). The postprandial response of inhibitory molecule from NF-kB mRNA levels increased with the HMUFA diet compared with the HSFA and LFHCC n-3 diets (p < 0.05). Postprandial tumor necrosis factor-α and Metalloproteinase 9 mRNA levels were also reduced after the HMUFA diet compared with the HSFA diet (p < 0.05).


CONCLUSIONS
Our results indicate that the long-term consumption of a healthy diet model with HMUFA attenuates the postprandial inflammatory state associated with MetS.
Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital/University of Cordoba and CIBER Fisiopatologia Obesidad y Nutricion (CIBEROBN), Instituto de Salud Carlos III, Córdoba, Spain.
Cristina
C
Cruz-Teno
Pablo
P
Pérez-Martínez
Javier
J
Delgado-Lista
Elena M
EM
Yubero-Serrano
Antonio
A
García-Ríos
Carmen
C
Marín
Purificación
P
Gómez
Yolanda
Y
Jiménez-Gómez
Antonio
A
Camargo
Fernando
F
Rodríguez-Cantalejo
Maria M
MM
Malagón
Francisco
F
Pérez-Jiménez
Helen M
HM
Roche
José
J
López-Miranda
D015331:Cohort Studies; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat / Q000009:adverse effects; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage / Q000627:therapeutic use; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage / Q000627:therapeutic use; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood / Q000235:genetics / Q000378:metabolism; D024821:Metabolic Syndrome / Q000097:blood / Q000178:diet therapy* / Q000276:immunology* / Q000378:metabolism; D008875:Middle Aged; D016328:NF-kappa B / Q000097:blood / Q000235:genetics / Q000378:metabolism; D010349:Patient Compliance; D019518:Postprandial Period; D012333:RNA, Messenger / Q000378:metabolism; D051996:Transcription Factor RelA / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics / Q000378:metabolism
D004041:Dietary Fats; D005229:Fatty Acids, Monounsaturated; D015525:Fatty Acids, Omega-3; D016328:NF-kappa B; C498143:RELA protein, human; D012333:RNA, Messenger; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D020780:Matrix Metalloproteinase 9