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Title: Jussara (Euterpe edulis Mart.) Supplementation during Pregnancy and Lactation Modulates the Gene and Protein Expression of Inflammation Biomarkers Induced by trans-Fatty Acids in the Colon of Offspring
Authors: Morais, Carina Almeida [UNIFESP]
Oyama, Lila Missae [UNIFESP]
Oliveira, Juliana Lopez de [UNIFESP]
Garcia, Marcia Carvalho [UNIFESP]
Rosso, Veridiana Vera de [UNIFESP]
Amigo, Laís Sousa Mendes [UNIFESP]
Nascimento, Claudia Maria da Penha Oller do [UNIFESP]
Pisani, Luciana Pellegrini [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 1-Jan-2014
Publisher: Hindawi Publishing Corporation
Citation: Mediators of Inflammation. New York: Hindawi Publishing Corporation, 11 p., 2014.
Abstract: Maternal intake of trans-fatty acids (TFAs) in the perinatal period triggers a proinflammatory state in offspring. Anthocyanins contained in fruit are promising modulators of inflammation. This study investigated the effect of Jussara supplementation in the maternal diet on the proinflammatory state of the colon in offspring exposed to perinatal TFAs. On the first day of pregnancy rats were divided into four groups: control diet (C), control diet with 0.5% Jussara supplementation (CJ), diet enriched with hydrogenated vegetable fat, rich in TFAs (T), or T diet supplemented with 0.5% Jussara (TJ) during pregnancy and lactation. We showed that Jussara supplementation inmaternal diet (CJ and TJ groups) reduced carcass lipid/protein ratios, serumlipids, glucose, IL-6, TNF-alpha, gene expression of IL-6R, TNF-alpha R (P < 0.05), TLR-4 (P < 0.01), and increase Lactobacillus spp. (P < 0.05) in the colon of offspring compared to the T group. the IL-10 (P = 0.035) and IL-10/TNF-alpha ratio (P < 0.01) was higher in the CJ group than in the T group. the 0.5% Jussara supplementation reverses the adverse effects of perinatal TFAs, improving lipid profiles, glucose levels, body composition, and gut microbiota and reducing low-grade inflammation in the colon of 21-day-old offspring, and could contribute to reducing chronic disease development.
ISSN: 0962-9351
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