Novel Adipokines CTRP1, CTRP9, and FGF21 in Pediatric Type 1 and Type 2 Diabetes: A Cross-Sectional Analysis

Alexander Arking1,2,3, Dylan C Sarver2,3, Sheela N Magge1

  • 1Department of Pediatric Endocrinology and Diabetes, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Insights

Novel adipokines CTRP9 and FGF21 show distinct patterns in pediatric diabetes. CTRP9 is higher in type 1 diabetes (T1D), while FGF21 is higher in type 2 diabetes (T2D), impacting metabolic homeostasis.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Pediatric Health

Background:

  • Rising rates of pediatric obesity and diabetes (type 1 and type 2) necessitate understanding novel biomarkers.
  • Limited knowledge exists on novel adipokines and hepatokines in pediatric diabetes populations.

Purpose of the Study:

  • To investigate the levels of novel adipokines C1q/TNF-related proteins (CTRP1 and CTRP9) and hepatokine fibroblast growth factor 21 (FGF21) in children with type 1 diabetes (T1D) and type 2 diabetes (T2D).
  • To assess the relationship between these novel adipokines and clinical characteristics in pediatric diabetes.

Main Methods:

  • Cross-sectional analysis of 80 participants (40 T1D, 40 T2D) from the Pediatric Diabetes Consortium (PDC) registries.
  • Comparison of CTRP1, CTRP9, and FGF21 levels between T1D and T2D cohorts.
  • Regression models to evaluate associations between adipokines and clinical parameters like C-peptide and hemoglobin A1c.

Main Results:

  • Participants with T2D had higher weight and BMI compared to T1D.
  • CTRP9 levels were significantly higher in youth with T1D than T2D (p=0.04).
  • FGF21 levels were significantly higher in youth with T2D than T1D (p=0.03).
  • In T1D, CTRP9 correlated with C-peptide, and FGF21 with hemoglobin A1c.
  • In T2D, CTRP1 correlated with hemoglobin A1c and glucose.

Conclusions:

  • Distinct patterns of CTRP9 and FGF21 exist between pediatric T1D and T2D.
  • These novel adipokines are associated with metabolic control in the inflammatory context of pediatric diabetes.
Abstract