Insulin Sensitivity and Insulin Secretion in Adults With Friedreich's Ataxia: The Role of Skeletal Muscle
Authors' conclusion
Lower mitochondrial OXPHOS capacity, inactivity, and visceral adiposity contribute to lower insulin sensitivity in FRDA. Higher insulin secretion appears compensatory and, when inadequate, could herald DM. Further studies are needed to determine if muscle- or adipose-focused interventions could delay FRDA-related DM.
Study context
- Population
- Adults with Friedreich's ataxia without diabetes mellitus (DM); Friedreich's ataxia (FRDA) median age 27 years (IQR 23, 39), BMI 26.9 kg/m²; controls 29 years (26, 39), BMI 24.4 kg/m²
- Participants
- 11 vs 24
- Comparison
- Adults with FRDA without DM vs controls
- FRDAn = 11
- Controlsn = 24reference
- Outcome
- Association between skeletal muscle health and insulin sensitivity and secretion
Main finding
As reported in the abstract
Insulin sensitivity (whole-body insulin sensitivity index)
FRDA
2.8
Controls
5.3
P < 0.01
Observational data: associations, not effects.
Further findings
Fasting glucose · higher with FRDA
P < 0.05
| Outcome | FRDA | Controls | P value |
|---|---|---|---|
| Postprandial insulin secretion (insulin secretory rate incremental AUC 30-180 minutes)Higher with FRDA | 24 652 | 17,858 | P < 0.05 |
| Postprandial endogenous glucose production (% of fasting)More suppressed with FRDA | −.9% | 26.9% | P < 0.05 |
Disposition index
- Insulin secretion accounting for sensitivity (disposition index) was not different
Original publication
Insulin Sensitivity and Insulin Secretion in Adults With Friedreich's Ataxia: The Role of Skeletal Muscle. J Clin Endocrinol Metab. Published 7 August 2024. doi:10.
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