Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents

Mosca, Antonella; Vito, Rita De; Crudele, Annalisa; Scorletti, Eleonora; Villani, Alberto; Alisi, Anna; Byrne, Christopher D.

doi:10.1016/j.jhep.2016.12.025

Cited by 160 publications

(130 citation statements)

References 29 publications

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“…Other studies have shown that rats fed a fructose-rich diet have increased hepatic triglyceride and cholesterol levels [42], and fructose fed to rodents at supraphysiological doses induced steatosis and steatohepatitis by de novo lipogenesis [43]. Meta-analyses have also suggested that fructose consumption is related to the risk factors for metabolic syndrome, such as increased triglyceride levels, stimulated hepatic de novo lipogenesis, and increased visceral fat [44,45,46,47]. …”

Section: Discussionmentioning

confidence: 99%

Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

et al. 2017

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Evidence indicates that many forms of fructose-induced metabolic disturbance are associated with oxidative stress and mitochondrial dysfunction. Mitochondria are prominent targets of oxidative damage; however, it is not clear whether mitochondrial DNA (mtDNA) damage and/or its lack of repair are events involved in metabolic disease resulting from a fructose-rich diet. In the present study, we evaluated the degree of oxidative damage to liver mtDNA and its repair, in addition to the state of oxidative stress and antioxidant defense in the liver of rats fed a high-fructose diet. We used male rats feeding on a high-fructose or control diet for eight weeks. Our results showed an increase in mtDNA damage in the liver of rats fed a high-fructose diet and this damage, as evaluated by the expression of DNA polymerase γ, was not repaired; in addition, the mtDNA copy number was found to be significantly reduced. A reduction in the mtDNA copy number is indicative of impaired mitochondrial biogenesis, as is the finding of a reduction in the expression of genes involved in mitochondrial biogenesis. In conclusion, a fructose-rich diet leads to mitochondrial and mtDNA damage, which consequently may have a role in liver dysfunction and metabolic diseases.

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Section: Discussionmentioning

confidence: 99%

Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

et al. 2017

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“…In a study of adolescents, hyperuricemia independently predicted [OR 2.5 (1.87–2.83)] the presence of NASH after adjusting for age, sex and other components of the metabolic syndrome (51). Hyperuricemia in males has also been found to associate more strongly with NASH than simple steatosis and was significantly associated with hepatocyte ballooning, BMI, and younger age in multivariate analysis (128).…”

Section: Fructokinase the Principal Enzyme Driving Fructose-induced mentioning

confidence: 99%

Fructose and sugar: A major mediator of non-alcoholic fatty liver disease

Jensen

Abdelmalek

Sullivan

et al. 2018

Journal of Hepatology

720

490

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Nonalcoholic Fatty Liver Disease (NAFLD) is the hepatic manifestation of metabolic syndrome, and its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high fructose corn syrup (HFCS)) not only increases the risk for NAFLD, but also, nonalcoholic steatohepatitis (NASH). Here we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked with metabolism of fructose by fructokinase C, resulting in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations in gut permeability, microbiome, and associated endotoxemia contributes to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.

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“…A high intake of dietary fructose is associated with NAFLD and, in addition, it has been shown that children with NAFLD absorb and metabolize fructose more effectively than normal-weight children [33,34]. Several studies have shown that children and adults with NAFLD have a higher mean fructose intake mainly resulting from a higher consumption of soft drinks and fruit juices as compared with subjects of same age without NAFLD [35,36].…”

Section: Other Impact To Healthmentioning

confidence: 99%

Consumption of Sugar-Sweetened Beverages in Paediatric Age: A Position Paper of the European Academy of Paediatrics and the European Childhood Obesity Group

Dereń

Weghuber

Caroli³

et al. 2019

Ann Nutr Metab

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Background: Health risks associated with the high consumption of sugar-sweetened beverages (SSBs) include overweight or obesity and their complications such as diabetes, as well as oral and dental decay, among others. Aim: The aim of the present statement is to inform health care professionals, parents, care-givers, teachers and school head teachers, stakeholders and governing bodies about the risks associated with drinking SSBs in infants, children and adolescents. Methods: We searched PubMed and the Cochrane databases for English language studies published from 2010 through October 1, 2018, for randomized clinical trials, meta-analyses, systematic reviews and observational studies (search terms are reported in eAppendix in the Supplement). We also manually searched the references of selected articles, reviews, meta-analyses and practice guidelines. Recommendations: Consumption of SSB by children and adolescents should be limited, and the consumption of water and other non-sweetened beverages should be promoted. Educational institutions such as nurseries, pre-schools and schools should offer unlimited access to drinking water, whereas the sale of SSBs should be banned.

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Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents

Cited by 160 publications

References 29 publications

Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats

Fructose and sugar: A major mediator of non-alcoholic fatty liver disease

Consumption of Sugar-Sweetened Beverages in Paediatric Age: A Position Paper of the European Academy of Paediatrics and the European Childhood Obesity Group

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