BIOACTIVITAT MOLECULAR DELS ALIMENTS (MOBIOFOOD)

Facultat de Química. Universitat Rovira i Virgili (URV)

Director: Maria Teresa Blay i Olivé
Adreça mail de contacte del grup de Recerca: mobiofood@urv.cat
Telèfon de contacte: +34  977 558497

Web del grup: http://www.bioactivity-food.recerca.urv.cat

Actualització fitxa tècnica del grup: gener 2020

MEMBRES DEL GRUP INVESTIGADOR

Anna Ardévol Grau
Catedràtic d’Universitat. Universitat Rovira i Virgili
anna.ardevol@urv.cat

Montserrat Pinent Armengol
Professora Agregada Serra Húnter. Universitat Rovira i Virgili
montserrat.pinent@urv.cat

Ximena Terra Barbadora.
Professora Lector Serra Húnter. Universitat Rovira i Virgili
ximena.terra@urv.cat

Raúl Beltrán Debón
Professor Lector Visitant. Universitat Rovira i Virgili
raul.beltran@urv.cat

Esther Rodríguez Gallego
Professor Lector Visitant. Universitat Rovira i Virgili
esther.rodriguez@urv.cat

Carlos A. González Quílen
Doctorand FI Generalitat de Catalunya. Universitat Rovira i Virgili
carlosalberto.gonzalez@urv.cat

Carme Grau Bové
Doctorand Martí Franques URV. Universitat Rovira i Virgili
carme.grau@urv.cat

Marta Sierra Cruz
Doctorand Martí Franques URV. Universitat Rovira i Virgili
marta.sierra@urv.cat

Alba Miguens Gómez
Doctorand Martí Franques URV. Universitat Rovira i Virgili
alba.miguens@urv.cat

Niurka Llópiz Janer
Tècnic Laboratori. Universitat Rovira i Virgili
niurkadariela.llopiz@urv.cat

ACTIVITATS I CAPACITATS DEL GRUP DE RECERCA

L’objectiu del grup de recerca és estudiar la bioactivitat molecular dels aliments a nivell de tracte gastrointestinal, es a dir, avaluar com diferents components de la nostra dieta poden afectar de manera adversa o beneficiosa el nostre intestí, i com aquesta interacció pot influencia la salut de la resta de l’organisme.

Actualment estem centrat en l’estudi de la interacció de components de la dieta amb el sistema enteroendocrí, la capacitat d’aquest compostos de modificar la integritat de la barrera intestinal i el se efecte immunomudoluador, així com l’estudi d’alteracions de la microbiota intestinal provocades per certs aliments, i finalment l’anàlisi dels efectes epigenètics de diferents compostos bioactius en situacions d’estrès metabòlic com són l’obesitat i/o l’envelliment.

LÍNIES DE RECERCA

Línia: INTERACCIÓ AMB RECEPTORS DE GUST I CONTROL DE LA INGESTA
Investigador principal/s: Anna Ardévol Grau

Línia: BIOACTIVITAT DELS COMPONENTS DE L’EXTRACTE DE PINYOL DE RAÏM O FONTS ALTERNATIVES DE PROTEÏNA DE RAÏM SOBRE A FUNCIÓ ENTEROENDOCRINA.
Investigador principal/s: Montserrat Pinent Armengol

Línia: BIOACTIVITAT DELS COMPONENTS DE L’EXTRACTE DE PINYOL DE RAÏM SOBRE LA INTEGRITAT DE LA BARRERA INTESTINAL
Investigador principal/s: Ximena Terra Barbadora

Línia: IMMUNOMODULACIÓ PRODUÏDA PEL CONSUM DE COMPONENTS DE L’EXTRACTE DE PINYOL DE RAÏM O DIFERENTS FONTS DE PROTEÏNA A NIVELL DE PARET INTESTINAL.
Investigador principal/s: MTeresa Blay Olivé

Línia: BIOACTIVITAD DE FONTS ALTERNATIVES DE PROTEÏNA SOBRE LA INTEGRITAT DE LA BARRERA INTESTINAL I L’ALTERACIÓ DE LA FUNCIONALITAT HEPÀTICA.
Investigador/s principal/s: Raul Beltran Debon/Esther Rodríguez Gallego

MILLORS PUBLICACIONS DEL GRUP (2017-2019)

Ginés I, Gil-Cardoso K, D’Addario C, Falconi A, Bellia F, Blay MT, Terra X, Ardévol A, Pinent M, Beltrán-Debón R.
Long-Lasting Effects of GSPE on Ileal GLP-1R Gene Expression Are Associated with a Hypomethylation of the GLP-1R Promoter in Female Wistar Rats.
Biomolecules. 2019 Dec 12;9(12). pii: E865.
doi: 10.3390/biom9120865
PMID: 31842341
Abstract

Flavonoids have been shown to modulate GLP-1 in obesity. GLP-1 induces some of its effects through the intestinal GLP-1 receptor (GLP-1R), though no data exist on how flavonoids affect this receptor. Here, we examine how a dose of grape seed proanthocyanidin extract (GSPE) with anti-obesity activity affects intestinal GLP-1R and analyze whether epigenetics play a role in the long-lasting effects of GSPE. We found that 10-day GSPE administration prior to the cafeteria diet upregulated GLP-1R mRNA in the ileum 17 weeks after the GSPE treatment. This was associated with a hypomethylation of the GLP-1R promoter near the region where the SP1 transcription factor binds. In the colon, the cafeteria diet upregulated GLP-1R without showing any GSPE effect. In conclusion, we have identified long-lasting GSPE effects on GLP-1R gene expression in the ileum that are partly mediated by hypomethylation at the gene promoter and may affect the SP1 binding factor.

Ginés I, Gil-Cardoso K, Terra X, Blay M, Pérez-Vendrell AM, Pinent M, Ardévol A.
Grape Seed Proanthocyanidins Target the Enteroendocrine System in Cafeteria-Diet-Fed Rats.
Mol Nutr Food Res. 2019 Jun;63(11):e1800912.
doi: 10.1002/mnfr.201800912.
PMID: 30980498
Abstract
SCOPE: The effects on the enteroendocrine system of three different grape seed proanthocyanidin extract (GSPE) treatments are analyzed in rats on a cafeteria diet for 17 weeks.
METHODS AND RESULTS: GSPE is administered in a corrective manner (15 last days of the cafeteria diet) at two doses, 100 and 500 mg GSPE per kg bw. A third, longer treatment in which GSPE (500 mg kg-1 bw) is administered daily every other week during the 17 weeks of the cafeteria diet is also tested. Most GSPE treatments lead to ghrelin accumulation in the stomach, limited CCK secretion in the duodenum, and increased GLP-1 and PYY mRNA in colon. GSPE also increases cecal hypertrophy and reduces butyrate content. When the treatment is administered daily every other week during 17 weeks, there is also an increase in colon size. These effects are accompanied by a reduced food intake at the end of the experiment when GSPE is administered at 500 mg GSPE kg-1 during the last 15 days, but not on the other treatments, despite an observed reduction in body weight in the longer treatment.
CONCLUSION: GSPE modulates the enteroendocrine system in models in which it also reduces food intake or body weight.

Gil-Cardoso K, Ginés I, Pinent M, Ardévol A, Blay M, Terra X.
The co-administration of proanthocyanidins and an obesogenic diet prevents the increase in intestinal permeability and metabolic endotoxemia derived to the diet.
J Nutr Biochem. 2018 Dec;62:35-42.
doi: 10.1016/j.jnutbio.2018.07.012.
PMID: 30245181
Abstract
The consumption of Westernized diets leads to hyperphagia and obesity, as well as intestinal alterations. In the present study, we evaluated the effect of the administration of a grape seed proanthocyanidin extract (GSPE) at different time points on the modulation of intestinal barrier function (intestinal permeability and metabolic endotoxemia), in rats with high-fat/high-carbohydrate diet-induced obesity. Animals were fed a cafeteria diet (CAF) supplemented with a preventive (PRE-CAF) or simultaneously intermittent (SIT-CAF) GSPE treatment (500 mg/kg bw). Changes in the plasma levels of an orally administered marker of intestinal permeability (ovalbumin, OVA), lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α) were analyzed after animals were fed the obesogenic diet for 8, 12 and 17 weeks. In addition, ex vivo variations in transepithelial electrical resistance (TEER), the expression of tight junction (TJ) genes and the activity of myeloperoxidase (MPO) in the small and large intestines were monitored at the end of the experiment. The CAF diet increased OVA, LPS, MPO and TNF-α levels, accompanied by decreased TEER values in the small and large intestines. Interestingly, both GSPE treatments prevented these detrimental effects of the CAF diet, being the SIT-CAF group the most effective after 17 weeks of diet intervention. For the first time, this study provides evidence of the ameliorative effect of a proanthocyanidin extract, administered before or together with an obesogenic diet, on barrier dysfunction, as measured by intestinal permeability and metabolic endotoxemia.

Olona A, Terra X, Ko JH, Grau-Bové C, Pinent M, Ardevol A, Diaz AG, Moreno-Moral A, Edin M, Bishop-Bailey D, Zeldin DC, Aitman TJ, Petretto E, Blay M, Behmoaras J.
Epoxygenase inactivation exacerbates diet and aging-associated metabolic dysfunction resulting from impaired adipogenesis.
Mol Metab. 2018 May;11:18-32.
doi: 10.1016/j.molmet.2018.03.003.
PMID: 29656108
Abstract
OBJECTIVE: When molecular drivers of healthy adipogenesis are perturbed, this can cause hepatic steatosis. The role of arachidonic acid (AA) and its downstream enzymatic cascades, such as cyclooxygenase, in adipogenesis is well established. The exact contribution of the P450 epoxygenase pathway, however, remains to be established. Enzymes belonging to this pathway are mainly encoded by the CYP2J locus which shows extensive allelic expansion in mice. Here we aimed to establish the role of endogenous epoxygenase during adipogenesis under homeostatic and metabolic stress conditions.
METHODS: We took advantage of the simpler genetic architecture of the Cyp2j locus in the rat and used a Cyp2j4 (orthologue of human CYP2J2) knockout rat in two models of metabolic dysfunction: physiological aging and cafeteria diet (CAF). The phenotyping of Cyp2j4-/- rats under CAF was integrated with proteomics (LC-MS/MS) and lipidomics (LC-MS) analyses in the liver and the adipose tissue.
RESULTS: We report that Cyp2j4 deletion causes adipocyte dysfunction under metabolic challenges. This is characterized by (i) down-regulation of white adipose tissue (WAT) PPARγ and C/EBPα, (ii) adipocyte hypertrophy, (iii) extracellular matrix remodeling, and (iv) alternative usage of AA pathway. Specifically, in Cyp2j4-/- rats treated with a cafeteria diet, the dysfunctional adipogenesis is accompanied by exacerbated weight gain, hepatic lipid accumulation, and dysregulated gluconeogenesis.
CONCLUSION: These results suggest that AA epoxygenases are essential regulators of healthy adipogenesis. Our results uncover their synergistic role in fine-tuning AA pathway in obesity-mediated hepatic steatosis.

Serrano J, Casanova-Martí À, Blay MT, Terra X, Pinent M, Ardévol A.
Strategy for limiting food intake using food components aimed at multiple targets in the gastrointestinal tract.
Trends in Food Science & Technology. 2017 Oct; 68: 113-129.
doi: 10.1016/j.tifs.2017.08.002

INSTITUCIONS QUE RECONEIXEN AL GRUP DE RECERCA

URV: Universitat Rovira i Virgili
XARTA: Xarxa de Referència en Tecnologia d’Aliments
Grup de Recerca Consolidat de l’AGAUR (2017 SGR 289)
IISPV: INSTITUT D’INVESTIGACIÓ SANITARIA: PERE VIRGILI