Differentiated Hepatic Response to Fructose Intake during Adolescence Reveals the Increased Susceptibility to Non‐Alcoholic Fatty Liver Disease of Maternal High‐Fat Diet Male Rat Offspring. Issue 3 (16th January 2020)

• Record Type: Journal Article
• Authors: Oliveira, Lorraine S.; Caetano, Bruna; Miranda, Rosiane A.; Souza, Aline F. P.; Cordeiro, Aline; Woyames, Juliana; Andrade, Cherley B. V.; Atella, Georgia C.; Takiya, Christina M.; Fortunato, Rodrigo S.; Trevenzoli, Isis H.; Souza, Luana L.; Pazos‐Moura, Carmen C.
• Is Part Of: Molecular nutrition & food research. Volume 64:Issue 3(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-01-16
• Subjects: adolescence -- fructose intake -- hepatic lipid metabolism -- maternal high‐fat diet -- oxidative stress; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201900838
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Scope: Non‐alcoholic fatty liver disease (NAFLD) among adolescents has been related to fructose intake. Additionally, maternal high‐fat diet (mHFD) increases the offspring susceptibility to NAFLD at adulthood. Here, it is hypothesized that mHFD may exacerbate the fructose impact in adolescent male rat offspring, by changing the response of contributing mechanisms to liver injury. Methods and results: Female Wistar rats receive standard (mSTD: 9% fat) or high‐fat diet (mHFD: 29% fat) prior mating throughout pregnancy and lactation. After weaning, offspring receive standard chow and, from the 25th to 45th day, receive water or fructose–drinking water (15%). At 46 days old, fructose groups show increased adiposity, increased serum and hepatic triglycerides, regardless of maternal diet. Fructose aggravates the hepatic imbalance of redox state already exhibited by mHFD offspring. The hepatic activation of cellular repair pathways by fructose, such as unfolded protein response and macroautophagy, is disrupted only in mHFD offspring. Fructose does not change the liver morphology of mSTD offspring. However, it intensifies the liver injury already present in mHFD offspring. Conclusion: Fructose intake during adolescence accelerates the emergence of NAFLD observed previously at the adult life of mHFD offspring, and reveals a differentiated hepatic response to metabolic insult, depending on the maternal diet. Abstract : In maternal standard diet (mSTD) adolescent offspring, fructose stress activates repair pathways, maintaining the redox balance and protecting the liver from injury. In maternal high‐fat diet (mHFD) offspring, the liver has oxidative stress (OS) and fructose stress leads to disruption on activation of hepatic repair pathways, impairing redox balance and favoring liver injury and development of non‐alcoholic fatty liver disease (NAFLD).