High Sucrose Intake Ameliorates the Accumulation of Hepatic Triacylglycerol Promoted by Restraint Stress in Young Rats.

IF 1.8 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Lipids Pub Date : 2015-11-01 Epub Date: 2015-09-23 DOI:10.1007/s11745-015-4066-0
Adriana Corona-Pérez, Mauricio Díaz-Muñoz, Ida Soto Rodríguez, Estela Cuevas, Margarita Martínez-Gómez, Francisco Castelán, Jorge Rodríguez-Antolín, Leticia Nicolás-Toledo
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引用次数: 14

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder. Stress promotes the onset of the NAFLD with a concomitant increment in the activity of the hepatic 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1). However, the interaction between the stress and a carbohydrate-enriched diet for the development of NAFLD in young animals is unknown. In the present study, we evaluated the impact of chronic stress on the hepatic triacylglycerol level of young rats fed or not with a high sucrose-diet. For doing this, 21-day old male Wistar rats were allocated into 4 groups: control (C), chronic restraint stress (St), high-sucrose diet (S30), and chronic restraint stress plus a 30 % sucrose diet (St + S30). Chronic restraint stress consisted of 1-hour daily session, 5 days per week and for 4 weeks. Rats were fed with a standard chow and tap water (C group) or 30 % sucrose diluted in water (S30 group). The St + S30 groups consumed less solid food but had an elevated visceral fat accumulation in comparison with the St group. The St group showed a high level of serum corticosterone and a high activity of the hepatic 11β-HSD-1 concomitantly to the augmentation of hepatic steatosis signs, a high hepatic triacylglycerol content, and hepatic oxidative stress. Conversely, the high-sucrose intake in stressed rats (St + S30 group) reduced the hepatic 11β-HSD-1 activity, the level of serum corticosterone, and the hepatic triacylglycerol content. Present findings show that a high-sucrose diet ameliorates the triacylglycerol accumulation in liver promoted by the restraint stress in young male rats.

高蔗糖摄取量可改善幼鼠抑制应激引起的肝脏甘油三酯积累。
非酒精性脂肪性肝病(NAFLD)是最常见的慢性肝病。应激促进NAFLD的发生,同时伴有肝脏11β-羟基类固醇脱氢酶1型(11β-HSD-1)活性的增加。然而,应激和富含碳水化合物的饮食之间的相互作用对幼年动物NAFLD的发展是未知的。在本研究中,我们评估了慢性应激对饲喂或不饲喂高蔗糖饮食的幼龄大鼠肝脏甘油三酯水平的影响。为此,将21日龄雄性Wistar大鼠分为4组:对照组(C)、慢性抑制应激(St)、高糖饮食(S30)和慢性抑制应激加30%蔗糖饮食(St + S30)。慢性约束压力包括每天1小时,每周5天,连续4周。用标准饲料加自来水(C组)或30%蔗糖水(S30组)喂养大鼠。St + S30组消耗较少的固体食物,但与St组相比,内脏脂肪积累增加。St组小鼠血清皮质酮水平升高,肝脏11β-HSD-1活性升高,同时肝脏脂肪变性体征增加,肝脏甘油三酯含量升高,肝脏氧化应激升高。相反,应激大鼠(St + S30组)高糖摄入降低了肝脏11β-HSD-1活性、血清皮质酮水平和肝脏甘油三酯含量。目前的研究结果表明,高糖饮食改善了年轻雄性大鼠由约束应激引起的肝脏甘油三酯积累。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Lipids
Lipids 生物-生化与分子生物学
CiteScore
4.20
自引率
5.30%
发文量
33
审稿时长
4-8 weeks
期刊介绍: Lipids is a journal of the American Oil Chemists'' Society (AOCS) that focuses on publishing high-quality peer-reviewed papers and invited reviews in the general area of lipid research, including chemistry, biochemistry, clinical nutrition, and metabolism. In addition, Lipids publishes papers establishing novel methods for addressing research questions in the field of lipid research.
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