Effect of high chronic intake of sucrose on liver metabolism in aging rats. Modulation by rutin and micronutrients
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ORIGINAL ARTICLE
Effect of high chronic intake of sucrose on liver metabolism in aging rats. Modulation by rutin and micronutrients Eva Gatineau 1 & Frédéric Capel 1 & Dominique Dardevet 1 & Jérémie David 1 & Corinne Pouyet 1 & Sergio Polakof 1 & Laurent Mosoni 1 Received: 4 October 2017 / Accepted: 3 April 2018 # University of Navarra 2018
Abstract High-sugar intake and senescence share common deleterious effects, in particular in liver, but combination of these two factors was little studied. Our aims were to examine the effect of a high-sucrose diet in liver of old rats and also the potential benefices of a polyphenol/micronutrient supplementation. Four groups of 22-month-old male rats fed during 5 months with a diet containing either 13 or 62% sucrose, supplemented or not with rutin, vitamin E, A, D, selenium, and zinc were compared. We measured liver macronutrient composition, glycation/oxidative stress, enzyme activities (lipogenesis, β-oxidation, fructokinase), gene expression (enzymes and transcription factors), in vivo protein synthesis rates and plasma parameters. Sucrose induced an increase in plasma and liver lipid content, and a stimulation of liver protein synthesis rates. Gene expression was little changed by sucrose, with lower levels for LXR-α and LXR-β. Polyphenol/micronutrient supplementation tended to limit liver triglyceride infiltration through variations in fatty acid synthase, acyl coA oxidase, and possibly ATP-citrate lyase activities. In conclusion, despite differences in enzymatic regulations, and blunted responses of gene expression, high-sucrose diet was still able to induce a marked increase in liver lipid content in old animals. However, it probably attenuated the positive impact of polyphenol/ micronutrients. Keywords Fructose . Polyphenols . Protein synthesis . Lipids . Triglycerides
Introduction Since the 1950s, added sugar consumption has been steadily increasing, leading to a high-fructose intake either in the form of sucrose (sucrose is half glucose, half fructose) or directly as pure fructose. It is thought to be responsible for many metabolic disorders [30]. Fructose triggers an increase in liver lipid content leading to insulin resistance, and then to dyslipidemia, hypertension, oxidative stress, inflammation, and non-alcoholic fatty liver disease [16]. The introduction in the 1970s of highfructose corn syrups boosted fructose consumption, which is now estimated at 10% of total energy intake [30]. Many studies were performed to analyze the consequences of such high-fructose intake, but most of them were performed
* Laurent Mosoni [email protected] 1
UNH, Unité de Nutrition Humaine, PFEM, MetaboHUB-Clermont, Université Clermont Auvergne, INRA, CRNH Auvergne, F-63000 Clermont-Ferrand, 63122 Theix, France
in young subjects. However, the proportion of elderly subjects increases in all countries. Since the 1950s, it is likely that sugar consumers are getting into old age and that they had a long-term high-fructose intake. Is it safe to superimpose the effects o
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