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

Oliveira, Lorraine S.; Caetano, Bruna; Miranda, Rosiane Aparecida; Souza, Aline F. P.; Cordeiro, Aline; Woyames, Juliana; Andrade, Cherley Borba Vieira de; Atella, Geórgia C.; Takiya, Christina Maeda; Fortunato, Rodrigo S.; Trevenzoli, Isis Hara; Souza, Luana Lopes; Pazos‐Moura, Carmen C.

doi:10.1002/mnfr.201900838

Cited by 14 publications

(18 citation statements)

References 45 publications

(52 reference statements)

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“…In addition, administration of the antioxidant lipoic acid or an inhibitor of NOX protects against fructose-induced hepatic insulin resistance, oxidative stress, and inflammation, reinforcing the relationship between hepatic oxidative stress and high fructose intake [308,310]. Fructose intake also enhances hepatic oxidative stress of maternal HFD offspring because of decline in the antioxidant defense system [311].…”

Section: Dietary Oxidants In Nafldmentioning

confidence: 96%

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

et al. 2020

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Non-alcoholic fatty liver disease (NAFLD) is often the hepatic expression of metabolic syndrome and its comorbidities that comprise, among others, obesity and insulin-resistance. NAFLD involves a large spectrum of clinical conditions. These range from steatosis, a benign liver disorder characterized by the accumulation of fat in hepatocytes, to non-alcoholic steatohepatitis (NASH), which is characterized by inflammation, hepatocyte damage, and liver fibrosis. NASH can further progress to cirrhosis and hepatocellular carcinoma. The etiology of NAFLD involves both genetic and environmental factors, including an unhealthy lifestyle. Of note, unhealthy eating is clearly associated with NAFLD development and progression to NASH. Both macronutrients (sugars, lipids, proteins) and micronutrients (vitamins, phytoingredients, antioxidants) affect NAFLD pathogenesis. Furthermore, some evidence indicates disruption of metabolic homeostasis by food contaminants, some of which are risk factor candidates in NAFLD. At the molecular level, several models have been proposed for the pathogenesis of NAFLD. Most importantly, oxidative stress and mitochondrial damage have been reported to be causative in NAFLD initiation and progression. The aim of this review is to provide an overview of the contribution of nutrients and food contaminants, especially pesticides, to oxidative stress and how they may influence NAFLD pathogenesis.

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Section: Dietary Oxidants In Nafldmentioning

confidence: 96%

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

et al. 2020

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“…Table 2 provides an overview of the study characteristics and outcome measures of the offspring effects. We extracted data from 18 studies that described 49 independent comparisons; however, not all necessary data for meta-analysis could be extracted from papers [ 23 , 25 , 30 – 42 , 45 , 46 ]. Out of 18 selected studies, ten [ 23 , 25 , 33 – 38 , 45 , 46 ] used rats (four Sprague–Dawley and six Wistar) and eight studies [ 30 – 32 , 34 , 39 – 41 , 43 ] used mice (C57BL/6).…”

Section: Resultsmentioning

confidence: 99%

“…We extracted data from 18 studies that described 49 independent comparisons; however, not all necessary data for meta-analysis could be extracted from papers [ 23 , 25 , 30 – 42 , 45 , 46 ]. Out of 18 selected studies, ten [ 23 , 25 , 33 – 38 , 45 , 46 ] used rats (four Sprague–Dawley and six Wistar) and eight studies [ 30 – 32 , 34 , 39 – 41 , 43 ] used mice (C57BL/6). Data from eleven studies were obtained from male offspring [ 30 – 33 , 37 – 40 , 42 , 43 , 46 ], and six studies used groups of mixed sex [ 25 , 34 – 36 , 41 , 45 ], whereas only one study represented data obtained from females [ 23 ].…”

Section: Resultsmentioning

confidence: 99%

“…Out of 18 selected studies, ten [ 23 , 25 , 33 – 38 , 45 , 46 ] used rats (four Sprague–Dawley and six Wistar) and eight studies [ 30 – 32 , 34 , 39 – 41 , 43 ] used mice (C57BL/6). Data from eleven studies were obtained from male offspring [ 30 – 33 , 37 – 40 , 42 , 43 , 46 ], and six studies used groups of mixed sex [ 25 , 34 – 36 , 41 , 45 ], whereas only one study represented data obtained from females [ 23 ]. The death age of the offspring was between one day after birth [ 25 ] and 650 days old [ 38 , 40 ].…”

Section: Resultsmentioning

confidence: 99%

“…Fat content in maternal HFD ranged from 29% [ 36 ] to 62% [ 41 ] calories from fat and the control group from 10 to 20%. The lard was the main fat component used by animal-derived fats in the twelve studies [ 23 , 25 , 30 , 33 , 36 – 39 , 41 , 43 , 45 , 46 ]; other two studies [ 34 , 35 ] used vegetal oils; and four studies did not report the fat component used [ 31 , 32 , 40 , 43 ]. The duration of maternal HFD exposure ranges from 19 [ 25 ] to 141 days [ 38 , 45 ], while the offspring HFD exposure ranges from 1 [ 25 , 35 , 40 ] to 650 postnatal day [ 38 , 45 ].…”

Section: Resultsmentioning

confidence: 99%

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Oxidative Stress Profile of Mothers and Their Offspring after Maternal Consumption of High‐Fat Diet in Rodents: A Systematic Review and Meta‐Analysis

Moraes-Souza

Vesentini

Paula

et al. 2021

Oxidative Medicine and Cellular Longevity

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Maternal exposure to the high-fat diet (HFD) during gestation or lactation can be harmful to both a mother and offspring. The aim of this systematic review was to identify and evaluate the studies with animal models (rodents) that were exposed to the high-fat diet during pregnancy and/or lactation period to investigate oxidative stress and lipid and liver enzyme profile of mothers and their offspring. The electronic search was performed in the PUBMED (Public/Publisher MEDLINE), EMBASE (Ovid), and Web of Science databases. Data from 77 studies were included for qualitative analysis, and of these, 13 studies were included for meta-analysis by using a random effects model. The pooled analysis revealed higher malondialdehyde levels in offspring of high-fat diet groups. Furthermore, the pooled analysis showed increased reactive oxygen species and lower superoxide dismutase and catalase in offspring of mothers exposed to high-fat diet during pregnancy and/or lactation. Despite significant heterogeneity, the systematic review shows oxidative stress in offspring induced by maternal HFD.

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Chronic Stress Potentiates High Fructose–Induced Lipogenesis in Rat Liver and Kidney

Milutinović

Brkljačić

Teofilović

et al. 2020

Molecular Nutrition Food Res

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Scope Intake of fructose‐sweetened beverages and chronic stress (CS) both increase risk of cardiometabolic diseases. The aim is to investigate whether these factors synergistically perturb lipid metabolism in rat liver and kidney. Methods and results Fractional de novo lipogenesis (fDNL), intrahepatic‐ and intrarenal‐triglycerides (IHTG and IRTG), de novo palmitate (DNPalm) content, FA composition, VLDL‐TGs kinetics, and key metabolic gene expression at the end of the feeding and non‐feeding phases in rats exposed to standard chow diet, chow diet + CS, 20% liquid high‐fructose supplementation (HFr), or HFr+CS are measured. HFr induces hypertriglyceridemia, up‐regulates fructose‐metabolism and gluconeogenic enzymes, increases IHTG and DNPalm content in IHTG and IRTG, and augments fDNL at the end of the feeding phase. These changes are diminished after the non‐feeding phase. CS does not exert such effects, but when combined with HFr, it reduces IHTG and visceral adiposity, enhances lipogenic gene expression and fDNL, and increases VLDL‐DNPalm secretion. Conclusion Liquid high‐fructose supplementation increases IHTG and VLDL‐TG secretion after the feeding phase, the latter being the result of stimulated hepatic and renal DNL. Chronic stress potentiates the effects of high fructose on fDNL and export of newly synthesized VLDL‐TGs, and decreases fructose‐induced intrahepatic TG accumulation after the feeding phase.

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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

Cited by 14 publications

References 45 publications

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants

Oxidative Stress Profile of Mothers and Their Offspring after Maternal Consumption of High‐Fat Diet in Rodents: A Systematic Review and Meta‐Analysis

Chronic Stress Potentiates High Fructose–Induced Lipogenesis in Rat Liver and Kidney

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