Dietary fructose: from uric acid to a metabolic switch in pediatric metabolic dysfunction-associated steatotic liver

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Maria Felicia Faienza1, Eleonora Cognetti1, Ilaria Farella2

  • 1Pediatric Unit, Department of Precision and Regenerative Medicine and Ionian Area, University of Bari "Aldo Moro", Bari, Italy.

Critical Reviews in Food Science and Nutrition
|August 19, 2024
PubMed

Insights

High fructose intake in children contributes to weight gain, insulin resistance, and fatty liver disease (MASLD/MASH). Reducing fructose intake can improve these metabolic health markers in pediatric subjects.

Area of Science:

  • Pediatric Endocrinology
  • Hepatology
  • Nutritional Science

Background:

  • Rising fructose consumption in children correlates with increased metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH).
  • Evidence links fructose to Metabolic Syndrome (MetS) and comorbidities, but its specific role in pediatric liver disease is not fully understood.
  • Fructose metabolism in the liver involves de novo lipogenesis (DNL) and uric acid accumulation, with hyperuricemia noted in MASLD patients.

Purpose of the Study:

  • To review the correlation between fructose metabolism and liver function in pediatrics.
  • To examine fructose's impact on childhood obesity, MASLD, and related metabolic dysfunctions.
  • To synthesize current evidence on fructose intake and liver health in children and adolescents.

Main Methods:

  • Narrative review of observational and interventional studies.
  • Inclusion of studies focusing on children and adolescents with high fructose and glucose intake.
  • Analysis of data linking dietary fructose to pediatric metabolic health outcomes.

Main Results:

  • Most studies show a strong association between high fructose intake and weight gain, dyslipidemia, insulin resistance, and MASLD/MASH in children, even normal-weight individuals.
  • Reduced fructose consumption demonstrated improvements in liver fat accumulation, lipid profiles, and body weight.
  • Fructose appears to be a significant factor in inducing insulin resistance and hepatic fat accumulation in pediatric populations.

Conclusions:

  • Fructose consumption is a key driver of insulin resistance and hepatic fat accumulation in children.
  • Dietary modification, specifically reducing fructose, offers a viable strategy to mitigate pediatric MASLD and metabolic dysfunction.
  • Further research is warranted to fully elucidate fructose's long-term impact on pediatric liver health and metabolic syndrome.

Keywords:
MASLDMetabolic syndromefructosepediatricuric acid

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