title: Postprandial changes in the proteome are modulated by dietary fat in patients with metabolic syndrome.
abstract: Metabolic syndrome is a multicomponent disorder whose etiology is the result of a complex interaction between genetic, metabolic and environmental factors including dietary habits. Our aim was to identify proteome-diet interactions during the postprandial state after the acute intake of four meals with different qualities of fat in the proteome of peripheral blood mononuclear cells. A randomized controlled trial conducted within the LIPGENE study assigned 39 metabolic syndrome patients to one of four meals: a high-saturated-fatty-acid (HSFA) meal, a high-monounsaturated-fatty-acid (HMUFA) meal and two high-polyunsaturated-fatty-acid (from walnut) (HPUFA) meals supplemented with n-3 PUFA or placebo. We analyzed the postprandial changes in the whole proteome of both nuclear and cytoplasmic fractions of peripheral blood mononuclear cells by two-dimensional proteomics. Twenty-three proteins were differentially expressed. HSFA intake caused the postprandial increase of proteins responding to oxidative stress (HSPA1A, PDIA3 and PSME1) and DNA damage (SMC6), whereas HMUFA intake led to the up-regulation of HSPA1A and PDIA3. HPUFA meal supplementation with n-3 PUFA produced peroxisomal beta-oxidation inhibition by down-regulation of ECH1, a process related to insulin signaling improvement. In conclusion, HSFA meal intake causes deleterious postprandial changes in the proteome in terms of DNA damage and procoagulant state, which reflect a higher postprandial oxidative stress after HSFA meal intake as compared to intake of HMUFA and HPUFA meals. Moreover, the addition of long-chain n-3 PUFA to an HPUFA meal may improve insulin signaling and exerts an anti-inflammatory effect when compared to an HPUFA meal.
authors.affiliation: Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital/University of Córdoba and CIBER Fisiopatología Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III. 14004, Córdoba, Spain.
authors.forename: Antonio
authors.initials: A
authors.lastname: Camargo
authors.forename: Oriol Alberto
authors.initials: OA
authors.lastname: Rangel-Zúñiga
authors.forename: Patricia
authors.initials: P
authors.lastname: Peña-Orihuela
authors.forename: Carmen
authors.initials: C
authors.lastname: Marín
authors.forename: Pablo
authors.initials: P
authors.lastname: Pérez-Martínez
authors.forename: Javier
authors.initials: J
authors.lastname: Delgado-Lista
authors.forename: Francisco Miguel
authors.initials: FM
authors.lastname: Gutierrez-Mariscal
authors.forename: María M
authors.initials: MM
authors.lastname: Malagón
authors.forename: Helen M
authors.initials: HM
authors.lastname: Roche
authors.forename: Francisco José
authors.initials: FJ
authors.lastname: Tinahones
authors.forename: Francisco
authors.initials: F
authors.lastname: Perez-Jimenez
authors.forename: José
authors.initials: J
authors.lastname: Lopez-Miranda
mesh_terms: D001798:Blood Proteins / Q000032:analysis / Q000378:metabolism; D015153:Blotting, Western; D004249:DNA Damage / Q000187:drug effects; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology*; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology; D006801:Humans; D031324:Juglans; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D024821:Metabolic Syndrome / Q000178:diet therapy / Q000378:metabolism*; D008875:Middle Aged; D019518:Postprandial Period / Q000187:drug effects*; D015203:Reproducibility of Results
chemical_list: D001798:Blood Proteins; D004041:Dietary Fats; D005229:Fatty Acids, Monounsaturated; D015525:Fatty Acids, Omega-3; D005231:Fatty Acids, Unsaturated