News|Articles|February 10, 2026

Experts urge for more research into youth-onset diabetes

Key Takeaways

  • Youth-onset type 2 diabetes has risen sharply since 2000, with childhood obesity identified as the primary and most modifiable risk factor worldwide.
  • Children show a higher genetic liability for type 2 diabetes than adults, with distinct genetic variants and disease pathways contributing to earlier and more severe metabolic dysfunction.
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A new review highlights how rising childhood obesity, genetic susceptibility, and early-life gut microbiota changes contribute to youth-onset type 2 diabetes.

Obesity, gut bacteria, and metabolic conditions in childhood and adolescence need additional investigation to protect children at risk of youth-onset diabetes, according to researchers from the University of Toronto.1

The research team highlighted a significant increase in the prevalence of youth-onset diabetes since 2000, noting obesity as a key risk factor. A 250% increase in child obesity rates has been reported in the past 3 decades, with a greater increase observed in low- and middle-income countries.

“Metabolic diseases in childhood, including type 2 diabetes, are modifiable and in some cases preventable — so it’s really important to understand the best ways to identify children who are at greater risk for metabolic dysfunction,” said Quin Xie, a research fellow at the University of Toronto.

Genetic contributions to type 2 diabetes risk in youth

To highlight the risk factors and mechanisms of type 2 diabetes (T2D) in children, the research team published a review in Cell Reports Medicine.2 The review included genetic studies which indicated a heritability of T2D ranging from 18% to 70%. Data has also indicated links with T2D for hundreds of loci, with some variants having greater effect sizes.

Noting the genes linked to T2D such as TCF7L2 and NEUROG3, investigators stated genetic factors may influence T2D through multiple tissues that increase adiposity or disrupt glucose absorption and regulation in the gut. Additionally, overlaps have been reported in the risk variants for coronary artery disease, peripheral artery disease, and end-stage diabetic nephropathy.

According to investigators, children have a greater genetic liability for T2D vs adults, especially for rare variants. Associations with monogenetic forms of diabetes have been observed for variants in HNF1A, MC4R, ATXN2L at the extreme end of the genetic risk spectrum. Reduced insulin production has also been reported for HNF1A variant.

This data highlights increased genetic risk burden and risk of metabolic compositions in youth-onset T2D. Therefore, researchers have concluded there are differences in pathogenesis vs adult-onset diabetes.

Obesity as the primary environmental risk factor

Investigators also highlighted environmental risk factors for T2D. Of these, obesity is the primary risk factor, significantly influencing insulin resistance and β-cell dysfunction. Data has also indicated a direct impact of increased caloric intake and reduced physical activity on microbial communities.

The gut microbiota mediates the link between environmental factors and metabolic functions in humans. Prior research has shown increased microbial capacity to degrade plant carbohydrates and produce short-chain fatty acids in humans with a fiber-rich Mediterranean diet and increased physical activity.

Rapid changes occur in the microbiota during the first 2 to 3 years of life, with Bifidobacterium predominance observed in this stage of life. Risks are often influenced by maternal factors, including a link between reduced exclusive breastfeeding and a distinct fecal microbiota composition at 1 month of age.

Prenatal and infant body mass index have also been linked to increased fungal richness in the first year of life. Based on these results, investigators recommended interventions for healthy colonization be utilized to reduce later obesity risk.

Limits and potential of gut microbiota–targeted interventions

Gut microbiota manipulation has yet to be decisively proven as effective for metabolic benefit. In a 3-month randomized clinical trial of 32 overweight and obese patients with insulin resistance, results were inconclusive.

Metabolic benefit was not observed from daily A. muciniphila doses, but aspects of metabolic dysfunction were improved, such as lower circulating insulin levels, reduced insulin resistance, and lower total blood cholesterol. Overall, this data indicated a need for obesity interventions to consider the impact of gut microbiota in treatment response and T2D risk.

“While the high prevalence of adult-onset T2D requires continued attention, global health priorities must expand to include young people and the primary disease driver—childhood obesity,” wrote investigators.

References

  1. Researchers urge focus on child obesity and gut health to reduce risk of diabetes. University of Toronto. February 4, 2026. Accessed February 9, 2026. https://www.eurekalert.org/news-releases/1115328
  2. Yuhui Xie Q, Jamilton JK, Danska JS. Gut microbiota and metabolic disease risk in youth. Cell Reports Medicine. 2026. doi:10.1016/j.xcrm.2025.102571

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