A major contributing factor is the nonphysiologic pattern of insulin replacement. In individuals without diabetes, endogenous insulin is secreted into the portal circulation and acts first on the liver. In contrast, in T1DM, subcutaneous insulin enters the systemic circulation directly, resulting in relatively higher peripheral insulin concentrations. This peripheral hyperinsulinemia promotes lipogenesis and suppresses lipolysis. Moreover, intensified insulin therapy has been consistently associated with gradual weight gain [2]. As body weight increases, insulin resistance rises, necessitating higher insulin doses. This creates a self-perpetuating cycle: higher insulin exposure promotes adiposity, and greater adiposity further increases insulin requirements.

Behavioral and developmental factors also contribute. Children and adolescents with T1DM frequently consume additional carbohydrates to prevent or treat hypoglycemia. Even with continuous glucose monitoring, fear of hypoglycemia often leads to defensive snacking. During puberty, growth hormone-mediated physiologic insulin resistance further increases insulin requirements. In an environment characterized by reduced physical activity and increased availability of energy-dense foods, these factors collectively make weight gain more likely [3].

Obesity in T1DM is not merely a consequence of treatment but may also influence disease biology. Kueh et al. [4] describe shared molecular pathways between obesity and T1DM, including chronic low-grade inflammation, lipotoxicity, and altered amino acid metabolism. Adipose tissue releases proinflammatory cytokines that impair insulin signaling and exacerbate insulin resistance. Some evidence suggests that a higher body mass index at diagnosis may be associated with more rapid β-cell decline, although this remains controversial [5]. Thus, obesity may both complicate established T1DM and potentially modify disease progression.

Lifestyle intervention remains the cornerstone of management. Structured nutrition counseling, caloric moderation, increased dietary fiber intake, and regular physical activity are essential components of care. However, lifestyle measures alone are often insufficient in adolescents with high insulin requirements and progressive weight gain. In such cases, adjunct pharmacologic therapy should be considered.

Metformin is the most extensively studied adjunctive agent in youth with T1DM. It improves insulin sensitivity and may modestly reduce insulin dose requirements and body mass index [6]. Although durable improvements in hemoglobin A1c have not been consistently demonstrated, metformin may help attenuate the cycle of hyperinsulinemia and weight gain in selected overweight adolescents with insulin resistance. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) offer a more targeted strategy for weight reduction. These agents reduce appetite, slow gastric emptying, and decrease postprandial glucose excursions. In adults with T1DM, adjunct GLP-1 therapy has been associated with weight loss and reduced total daily insulin dose [7]. Although pediatric data remain limited, GLP-1 RAs are approved for adolescent obesity and have an expanding safety profile. In carefully selected youth with T1DM and obesity, they may facilitate caloric reduction and insulin dose adjustment. Close monitoring is required to minimize the risk of ketosis when insulin doses are reduced. Sodium–glucose cotransporter- 2 inhibitors have demonstrated weight and glycemic benefits in adults with T1DM, but the risk of euglycemic diabetic ketoacidosis has limited their application in pediatric practice [7]. Until robust safety data are available in children and adolescents, routine use in pediatric T1DM is not recommended.

The global burden of T1DM continues to increase, as reported in the 2025 International Diabetes Federation Atlas and T1DM Index update [8]. As survival improves and disease duration lengthens, the overlap between T1DM and obesity is likely to expand. This evolving phenotype requires a shift in clinical priorities. Assessment of waist circumference, lipid profile, blood pressure, liver enzymes, and markers of insulin resistance should be integrated into routine care for overweight youth with T1DM [9].

In summary, I also agree with the issues and results from the study by Wong et al. [1]. Obesity in pediatric T1DM arises from a complex interplay of nonphysiologic insulin exposure, behavioral adaptations to hypoglycemia, pubertal insulin resistance, and adipose-driven inflammation. It accelerates insulin resistance and amplifies cardiovascular risk from an early age. Effective management requires more than glycemic control alone. Early weight management, careful insulin optimization, and appropriate adjunct pharmacotherapy may reduce long-term vascular complications and improve overall metabolic health in children and adolescents living with T1DM.