Long-term exposure to high-sucrose diet down-regulates hepatic endoplasmic reticulum-stress adaptive pathways and potentiates de novo lipogenesis in weaned male mice

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Arquivos
art_FLISTER_Longterm_exposure_to_highsucrose_diet_downregulates_hepatic_endoplasmic_2018.PDF (3.61 MB)
Citações na Scopus
24
Tipo de produção
article
Data de publicação
2018
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCIENCE INC
Autores
FLISTER, Karla Frida Torres
PINTO, Bruno Araujo Serra
FRANCA, Lucas Martins
COELHO, Caio Fernando Ferreira
SANTOS, Pamela Costa dos
VALE, Caroline Castro
PAES, Antonio Marcus de Andrade
Citação
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, v.62, p.155-166, 2018
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Childhood consumption of added sugars, such as sucrose, has been associated to increased risk of metabolic syndrome (MetS) and nonalcoholic fatty liver disease (NAFLD). Although the mechanisms underlying NAFLD onset are incompletely defined, recent evidence has proposed a role for the endoplasmic reticulum (ER) stress. Thus, the present study sought to investigate the metabolic outcomes of high-sucrose intake on weaned Swiss mice fed a 25% sucrose diet for 30, 60 and 90 days in comparison to regular chow-fed controls. High-sucrose feeding promoted progressive metabolic and oxidative disturbances, starting from fasting and fed hyperglycemia, hyperinsulinemia, glucose intolerance and increased adiposity at 30-days; passing by insulin resistance, hypertriglyceridemia and NAFLD onset at 60 days; until late hepatic oxidative damage at 90 days. In parallel, assessment of transcriptional and/or translational levels of de novo lipogenesis (DNL) and ER stress markers showed up-regulation of both fatty acid synthesis (ChREBP and SCD1) and oxidation (PPAR alpha and CPT-1 alpha), as well as overexpression of unfolded protein response sensors (IRE1 alpha, PERK and ATF6), chaperones (GRP78 and PDIA1) and antioxidant defense (NRF2) genes at 30 days. At 60 days, fatty acid oxidation genes were down-regulated, and ER stress switched over toward a proapoptotic pattern via up-regulation of BAK protein and CHOP gene levels. Finally, down-regulation of both NRF2 and CPT-1 alpha protein levels led to late up-regulation of SREBP-1c and exponential raise of fatty acids synthesis. In conclusion, our study originally demonstrates a temporal relationship between DNL and ER stress pathways toward MetS and NAFLD development on weaned rats fed a high-sucrose diet.
Palavras-chave
Nonalcoholic fatty liver disease, Endoplasmic reticulum stress, De novo lipogenesis, High-sucrose diet, Microvesicular steatosis, Metabolic syndrome
URI
https://observatorio.fm.usp.br/handle/OPI/30252
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Coleções
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - FM/MCP
Artigos e Materiais de Revistas Científicas - LIM/19