ESPE Abstracts

Background: Puberty is a time of hormonal changes that are associated with insulin resistance. Although insulin sensitivity is restored at the end of puberty in healthy youth, it does not resolve in obese adolescents leading to an increase of cardio metabolic disease such as type 2 diabetes. In response to an increase in insulin demand, as during pregnancy or obesity-induced insulin resistance, β-cells increase their functional mass to maintain glucose homeostasis. However, the mechanism of pancreatic β-cell compensation in the face of pubertal insulin resistance has not been established. Hormonal changes during puberty could be linked to this β-cell adaptation.

Objective: To characterize pancreatic β-cell adaptation to pubertal insulin-resistance.

Methods: Metabolic (body weight, fasted plasma insulin, glucose tolerance) and hormonal (vaginal opening, estradiol, testosterone, IGF1 levels) parameters were measured in Wistar rats from weaning to adulthood. β-cell proliferation was assessed by immunostaining of pancreatic cryosections for Ki67 and insulin to mark β-cells and β-cell mass by morphometric analysis of insulin staining.

Results: As expected we observed glucose intolerance and an increase in insulin levels during puberty in female and male rats, suggesting increased insulin resistance. An increase in β-cell proliferation at puberty was found, interestingly correlated with the rise in IGF1 levels rather than sex steroids.

Conclusion: Insulin resistance and β-cell proliferation increase during puberty in rats. The parallel increase in IGF1 levels and β-cell proliferation point to a possible role of growth hormone in compensatory β-cell expansion. In future studies we will assess whether β-cell adaptation is compromised in a pathological model of metabolic stress during puberty.