Literature DB >> 26399510

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

Adriana Corona-Pérez1, Mauricio Díaz-Muñoz2, Ida Soto Rodríguez3, Estela Cuevas4, Margarita Martínez-Gómez4,5, Francisco Castelán4, Jorge Rodríguez-Antolín4, Leticia Nicolás-Toledo6.   

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.

Entities:  

Keywords:  Corticosterone; Hepatic 11β-hydroxysteroid dehydrogenase type 1; Non-alcoholic fatty liver disease; Oxidative stress; Visceral fat

Mesh:

Substances:

Year:  2015        PMID: 26399510     DOI: 10.1007/s11745-015-4066-0

Source DB:  PubMed          Journal:  Lipids        ISSN: 0024-4201            Impact factor:   1.880


  61 in total

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