Literature DB >> 28969511

Interactive effects of chronic stress and a high-sucrose diet on nonalcoholic fatty liver in young adult male rats.

Adriana Corona-Pérez1, Mauricio Díaz-Muñoz2, Estela Cuevas-Romero3, Dalia Luna-Moreno4, Héctor Valente-Godínez2, Olivia Vázquez-Martínez2, Margarita Martínez-Gómez3,5, Jorge Rodríguez-Antolín3, Leticia Nicolás-Toledo3.   

Abstract

Glucocorticoids have been implicated in nonalcoholic fatty liver diseases (NAFLD). The influence of a palatable diet on the response to stress is controversial. This study explored whether a high-sucrose diet could protect from hepatic steatosis induced by chronic restraint stress in young adult rats. Male Wistar rats aged 21 days were allocated into four groups (n = 6-8 per group): control, chronic restraint stress, 30% sucrose diet, and 30% sucrose diet plus chronic restraint stress. After being exposed to either tap water or sucrose solution during eight weeks, half of the rats belonging to each group were subject or not to repeated restraint stress (1 h per day, 5 days per week) during four weeks. Triacylglycerol (TAG), oxidative stress, activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1), infiltration of immune cells, and glycogen amount in the liver were quantified. Serum concentrations of corticosterone and testosterone were also measured. The stressed group showed normal serum concentrations of corticosterone and did not have hepatic steatosis. However, this group showed increased glycogen, inflammation, mild fibrosis, oxidative stress, and a high activity of 11β-HSD-1 in the liver. The group exposed to the high-sucrose diet had lower concentrations of corticosterone, hepatic steatosis and moderate fibrosis. The group subject to high-sucrose diet plus chronic restraint stress showed low concentrations of corticosterone, hepatic steatosis, oxidative stress, and high concentrations of testosterone. Thus, restraint stress and a high-sucrose diet each generate different components of nonalcoholic fatty liver in young adult rats. The combination of both the factors could promote a faster development of NAFLD.

Entities:  

Keywords:  11β-HSD-1; NAFLD; corticosterone; hepatic fibrosis; hepatic steatosis; oxidative stress

Mesh:

Substances:

Year:  2017        PMID: 28969511     DOI: 10.1080/10253890.2017.1381840

Source DB:  PubMed          Journal:  Stress        ISSN: 1025-3890            Impact factor:   3.493


  4 in total

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