Apelin and Myostatin Levels in Adolescents With Type-1-Diabetes

Area of Science:

• Endocrinology
• Metabolic Research
• Muscle Physiology

Background:

• Myokines, secreted by skeletal muscle, influence metabolic function and inter-tissue communication.
• While myokines are implicated in obesity and type 2 diabetes (T2D), their role in type 1 diabetes (T1D) remains under-investigated.
• Skeletal muscle dysfunction may contribute to T1D pathogenesis.

Purpose of the Study:

• To investigate serum levels of five key myokines (Apelin, Irisin, IL-6, FGF21, Myostatin) in adolescents with T1D.
• To compare myokine levels between recent-onset T1D, prolonged T1D (over 7 years), and healthy controls.
• To explore the clinical correlates of these myokines, including metabolic parameters and diabetes management indicators.

Main Methods:

• Cross-sectional study involving 58 adolescents: 20 with recent-onset T1D, 20 with prolonged T1D, and 18 healthy controls.
• Measurement of serum levels for Apelin, Irisin, Interleukin-6 (IL-6), Fibroblast growth factor 21 (FGF21), and Myostatin.
• Collection of clinical data, including C-peptide levels, insulin dosage, and diastolic blood pressure (BP) percentile.

Main Results:

• Apelin levels were significantly lower in adolescents with prolonged T1D compared to recent-onset T1D and controls (p=0.029).
• No significant differences were observed in Irisin, IL-6, or FGF21 levels between the groups.
• Apelin levels correlated positively with fasting C-peptide (p=0.010). Myostatin positively correlated with insulin doses (p=0.006-0.002) in prolonged T1D.
• Both apelin and myostatin levels showed negative correlations with diastolic BP percentile (p=0.013 and p=0.024, respectively).

Conclusions:

• Adolescents with prolonged T1D exhibit reduced levels of apelin, a myokine associated with favorable metabolic effects.
• The observed correlations suggest potential links between apelin, residual beta-cell function (C-peptide), and myostatin with insulin sensitivity and diabetes management.
• These findings highlight the potential involvement of myokine dysregulation in the pathophysiology of long-standing T1D.