A mix of dietary fermentable fibers improves lipids handling by the liver of overfed minipigs

Obesity induced by overfeeding ultimately can lead to nonalcoholic fatty liver disease, whereas dietary fiber consumption is known to have a beneficial effect. We aimed to determine if a supplementation of a mix of fibers (inulin, resistant starch and pectin) could limit or alleviate overfeeding-ind...

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Published inThe Journal of nutritional biochemistry Vol. 65; pp. 72 - 82
Main Authors Mohamed, Ahmed Ben, Rémond, Didier, Chambon, Christophe, Sayd, Thierry, Hébraud, Michel, Capel, Frédéric, Cohade, Benoit, Hafnaoui, Noureddine, Béchet, Daniel, Coudy-Gandilhon, Cécile, Migné, Carole, David, Jeremie, Dardevet, Dominique, Doré, Joel, Polakof, Sergio, Savary-Auzeloux, Isabelle
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.03.2019
Elsevier
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Summary:Obesity induced by overfeeding ultimately can lead to nonalcoholic fatty liver disease, whereas dietary fiber consumption is known to have a beneficial effect. We aimed to determine if a supplementation of a mix of fibers (inulin, resistant starch and pectin) could limit or alleviate overfeeding-induced metabolic perturbations. Twenty female minipigs were fed with a control diet (C) or an enriched fat/sucrose diet supplemented (O + F) or not (O) with fibers. Between 0 and 56 days of overfeeding, insulin (+88%), HOMA (+102%), cholesterol (+45%) and lactate (+63%) were increased, without any beneficial effect of fibers supplementation. However, fibers supplementation limited body weight gain (vs. O, −15% at D56) and the accumulation of hepatic lipids droplets induced by overfeeding. This could be explained by a decreased lipids transport potential (−50% FABP1 mRNA, O + F vs. O) inducing a down-regulation of regulatory elements of lipids metabolism / lipogenesis (−36% SREBP1c mRNA, O + F vs. O) but not to an increased oxidation (O + F not different from O and C for proteins and mRNA measured). Glucose metabolism was also differentially regulated by fibers supplementation, with an increased net hepatic release of glucose in the fasted state (diet × time effect, P<.05 at D56) that can be explained partially by a possible increased glycogen synthesis in the fed state (+82% GYS2 protein, O + F vs. O, P=.09). The direct role of short chain fatty acids on gluconeogenesis stimulation is questioned, with probably a short-term impact (D14) but no effect on a long-term (D56) basis.
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ISSN:0955-2863
1873-4847
DOI:10.1016/j.jnutbio.2018.12.002