Liver zonation in children with non‐alcoholic fatty liver disease: Associations with dietary fructose and uric acid concentrations

Nobili, Valério; Vito, Rita De; Raponi, Massimiliano; Scorletti, Eleonora; Byrne, Christopher D.

doi:10.1111/liv.13661

Cited by 22 publications

(22 citation statements)

References 36 publications

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“…In line with recent cross-sectional studies in adults (145, 146), Vos et al (147) examined the relationship between SUA levels and NAFLD in the pediatric population, reporting that uric acid was significantly increased in those children with histological diagnosis of NASH compared with milder forms of NAFLD. In accordance with the latest study, Nobili et al (148) have recently observed that hyperuricemia, coupled with elevated dietary fructose consumption, could be responsible for the different pattern of lobular disease observed in pediatric NAFLD, determining greater damage in the periportal zone rather than in perivenous zone (148). Similarly, in a pilot study by Sullivan et al (149) children with NAFLD after fructose ingestion reported an exacerbated metabolic profile characterized by elevated serum glucose, insulin, and uric acid associated with an higher urinary levels of uric acid and a lower fructose excretion than lean subjects.…”

Section: Common Pathogenetic Mechanisms Linking Nafld and Metssupporting

confidence: 73%

The Liver in Children With Metabolic Syndrome

2019

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Non-alcoholic fatty liver disease (NAFLD) is recognized as an emerging health risk in obese children and adolescents. NAFLD represents a wide spectrum of liver conditions, ranging from asymptomatic steatosis to steatohepatitis. The growing prevalence of fatty liver disease in children is associated with an increased risk of metabolic and cardiovascular complications. NAFLD is considered the hepatic manifestation of Metabolic Syndrome (MetS) and several lines of evidence have reported that children with NAFLD present one or more features of MetS. The pathogenetic mechanisms explaining the interrelationships between fatty liver disease and MetS are not clearly understood. Altough central obesity and insulin resistance seem to represent the core of the pathophysiology in both diseases, genetic susceptibility and enviromental triggers are emerging as crucial components promoting the development of NAFLD and MetS in children. In the present review we have identified and summarizied studies discussing current pathogenetic data of the association between NAFLD and MetS in children.

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Section: Common Pathogenetic Mechanisms Linking Nafld and Metssupporting

confidence: 73%

The Liver in Children With Metabolic Syndrome

2019

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“…Chronic fructose ingestion, most notably in industrialized countries, has contributed to increasing prevalence of obesity and a myriad of chronic health conditions, including those involved with metabolic syndrome,7,13,14 that have produced a substantial economic and medical burden on our healthcare system 13,15. In particular, the hepatic consequences of metabolic syndrome have led to negative outcomes and continue to be a subject matter of interest 6,16,17…”

Section: Fructose In Diet and Healthcare Burdenmentioning

confidence: 99%

<p>The negative and detrimental effects of high fructose on the liver, with special reference to metabolic disorders</p>

Brandon

2019

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The increased consumption of fructose in the average diet through sweeteners such as high-fructose corn syrup (HFCS) and sucrose has resulted in negative outcomes in society through producing a considerable economic and medical burden on our healthcare system. Ingestion of fructose chronically has contributed to multiple health consequences, such as insulin resistance, obesity, liver disorders, and diabetes. Fructose metabolism starts with fructose phosphorylation by fructose kinase in the liver, and this process is not feedback regulated. Therefore, ingestion of high fructose can deplete ATP, increase uric acid production, and increase nucleotide turnover. This review focuses the discussion on the hepatic manifestations of high fructose-implicated liver metabolic disorders such as insulin resistance, obesity due to enhanced lipogenesis, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and type 2 diabetes. The detrimental effects of high fructose on the liver, contributed potentially by microbiome and leptin, were also discussed. The authors believe that, together with diet management, further studies focusing on disrupting or blocking fructose metabolism in the liver may help with designing novel strategies for prevention and treatment of fructose-induced chronic liver metabolic diseases.

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“…This is supported by the finding of increased steatosis in the portal area in rats fed with both sucrose and fructose‐enriched diets . Similarly, Nobili et al recently showed that high‐fructose intake in children correlated with increased portal steatosis, inflammation and hypothesis …”

Section: Paediatric Nafldmentioning

confidence: 72%

A narrative review of factors associated with the development and progression if non‐alcoholic fatty liver disease

et al. 2019

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Summary Background With the obesity pandemic, non‐alcoholic fatty liver disease (NAFLD) has become the most prevalent liver disease. NAFLD can progress to non‐alcoholic steatohepatitis (NASH), a potential cause of liver failure. It remains difficult to identify patients at risk for NASH, despite evolving insights in contributing factors, including genetic variance, hormones, adipokines, diet and body‐fat distribution. We aimed to present a broad perspective on these risk factors associated with NAFLD development and progression with a focus on their contribution in different age groups and susceptible high‐risk populations, hereby giving insight in the pathophysiology of NAFLD. Methods Literature was searched for relevant articles on the pathophysiology of NAFLD in different age groups. Results Our review underscores large contributions of diet, with particularly fructose promoting NASH development, and sex hormones, with oestrogens exerting protective effects and androgens negatively influencing NAFLD development. Genetic variation in corresponding pathways might further determine NAFLD progression. Conclusions Changes throughout the transition from childhood to adulthood show that variations in diet, hormone levels and metabolism are related to NAFLD progression. The human body uses different strategies to handle excessive nutrients, but each comes at a price. When corresponding pathways are strained by hormonal or genetic factors, NASH or other symptoms of the metabolic syndrome ensue. Potentially, stratification based on sex, body‐fat distribution, diet, lifestyle, microbiome, adipokines, sex hormones, blood concentrations of liver enzymes, liver histology and genetic pre‐disposition might help to identify patients at increased risk of NASH.

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Liver zonation in children with non‐alcoholic fatty liver disease: Associations with dietary fructose and uric acid concentrations

Abstract: High fructose consumption is associated with disease severity in both lobular zones and hyperuricaemia may be associated with more severe disease in the periportal zone.

Cited by 22 publications

References 36 publications

The Liver in Children With Metabolic Syndrome

The Liver in Children With Metabolic Syndrome

<p>The negative and detrimental effects of high fructose on the liver, with special reference to metabolic disorders</p>

A narrative review of factors associated with the development and progression if non‐alcoholic fatty liver disease

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