The metabolic toll of sweetness: fructose and the global rise in childhood health risks. A critical review
Year: 2025
Type: article
Abstract: As the global rise in pediatric metabolic dysfunction continues, mounting evidence implicates excessive intake of added sugars – particularly fructose – as a primary metabolic disruptor. This critical review examines the metabolic impact of high fructose intake during childhood, drawing from current findings in nutritional biochemistry, pediatric endocrinology and public health. Unlike glucose, fructose is primarily metabolized in the liver, where it bypasses key regulatory steps of glycolysis, leading to unregulated phosphorylation by ketohexokinase C (KHK-C). This drives rapid ATP depletion and uric acid production, initiating mitochondrial dysfunction, oxidative stress and de novo lipogenesis. These processes contribute to the early onset of metabolic syndrome, serving as initiating mechanisms for the development of insulin resistance, visceral adiposity, hepatic steatosis and metabolic dysfunction – associated steatotic liver disease (MASLD). Furthermore, fructose metabolism promotes systemic inflammation through immune activation, oxidative stress and gut microbiota disruption, factors that amplify the metabolic dysfunction and the long-term disease risk. Fructose has also been implicated in neuroinflammatory pathways, altered appetite regulation and intestinal barrier impairment. This review underscores the need for early intervention strategies, including sugar taxation, improved food labeling, nutritional education and clinical counseling. Reducing pediatric fructose exposure represents a critical, equity-driven priority for mitigating long-term metabolic risks and for promoting population health.
Source: Pediatru ro
Institution: Grigore T. Popa University of Medicine and Pharmacy
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
OpenAlex ID: W4412954855