ESPE Yearbook of Paediatric Endocrinology

Brief summary: This longitudinal study aimed to determine if hyperinsulinemia and postprandial glucose levels could predict obesity progression in n=591 children and adolescents with obesity. The authors found no association between hyperinsulinemia, insulin secretion, low postprandial glucose levels, and an increase in obesity over a 2–4-year period.

According to the carbohydrate-insulin model (1), diets with a high glycemic load (GL) promote weight gain by increasing the ratio of insulin-to-glucagon in the blood, resulting in an anabolic state that promotes fat deposition and reduces available calories for energy expenditure. As a result, there is an increase in hunger while the body may reduce its energy expenditure in an effort to maintain energy balance. Studies in adults have shown a correlation between insulin secretion and weight gain (2), and a genetic study using a Mendelian-randomization approach suggested a potentially causal relationship between genetically determined insulin secretion and higher BMI (3).

However, limited data exist for the carbohydrate-insulin model in children. The results of the present study indicate that numerous indices of hyperinsulinemia (including area under the curve of insulin, peak insulin, fasting insulin, insulinogenic index, and insulin at 30 minutes) were not associated with greater increases in the degree of obesity over a follow-up period of 2–4 years. Additionally, low postprandial glucose levels were not linked to increased obesity progression. These findings suggest that, in children and adolescents with obesity, exposure to hyperinsulinemia or greater insulin secretion is not a significant driver of obesity progression over the short to medium term, therefore challenging the assumptions of the carbohydrate-insulin model. The study has several noteworthy strengths, including the inclusion of a relatively large and diverse sample, the incorporation of a high-risk group, and the investigation of multiple physiologically relevant aspects of insulin dynamics. However, there are also some limitations to consider. These include potential issues with the validity of insulin assays used, the lack of dietary data to assess the effect of glycemic load on insulin dynamics, and the relatively short duration of follow-up compared to other studies.

In conclusion, Halloun et al. contribute to our understanding of nutrition and the role of insulin secretion in weight gain among children and adolescents. However, more research is needed to provide a comprehensive assessment of the relationship between insulin dynamics, dietary factors, and long-term weight outcomes in children.

References: 1. Ludwig DS, Aronne LJ, Astrup A, et al. The carbohydrate-insulin model: a physiological perspective on the obesity pandemic. Am J Clin Nutr 2021;114:1873–1885. 2. Sigal RJ, El-Hashimy M, Martin BC, Soeldner JS, Krolewski AS, Warram JH. Acute postchallenge hyperinsulinemia predicts weight gain: a prospective study. Diabetes 1997;46:1025–1029. 3. Astley CM, Todd JN, Salem RM, et al. Genetic evidence that carbohydrate-stimulated insulin secretion leads to obesity. Clin Chem 2018;64:192–200.