1165-P: Untangling the Interactions of Glycemic Control and Obesity on Hypothalamic Gliosis in Youth with Type 1 Diabetes

Introduction and Objective: Adolescents and young adults (AYA) with T1D experience high rates of disordered eating behavior (DEB), and obesity, which are linked to worse health outcomes including glycemic control. Inflammatory changes in the brain such as gliosis specifically in the mediobasal hypothalamus (MBH) -a critical area for weight regulation- may contribute. Adults with T2D have greater MBH gliosis compared to those with impaired glucose tolerance or normoglycemia, independent of adiposity. We investigated the presence of MBH gliosis in AYA with T1D and assessed its association with adiposity and glycemic control.

Methods: We recruited females aged 15-25 years; 24 with T1D and 5 healthy controls. AYA with T1D had stable insulin regimens and had diabetes duration for at least 1 year. Those with history of serious chronic conditions, eating disorder, extreme fluctuations in weight or glycemic control were excluded. Participants completed fasting labs, DEB surveys, DEXA scan and multi-echo brain MRI. T2 relaxation time (a measure for gliosis) was quantified in the MBH and control regions: amygdala (AMY) and putamen (PUT). Linear regression tested if T2 relaxation time in brain regions of interest were associated with body mass index (BMI) and HbA1c.

Results: For those with T1D, diabetes duration was 8.9±2.8 y and mean HbA1c was 7.9 ±1.7% (range 5.7 to 11.8%). 10 were lean and 14 had overweight or obesity based on BMI. There was a positive trend between MBH T2 relaxation time and BMI but not for other brain regions (MBH p=0.12; R = 0.28; AMY p=0.26, R=0.22; PUT p=0.30, R=0.2). There was no association between HbA1c and T2 relaxation in all brain regions (MBH p=0.88, R=0.3; AMY p=0.79, R= 0.05; PUT p=0.93, R=0.01).

Conclusion: We observed a trend that suggests that BMI but not HbA1c may be associated with MBH gliosis in AYA with T1D. Although glycemic control is associated with MBH gliosis in adults with T2D or insulin resistance, this relationship may not be present in AYA with T1D.