Observational studyThe Journal of clinical endocrinology and metabolism2025
Insulin Sensitivity and Insulin Secretion in Adults With Friedreich's Ataxia: The Role of Skeletal Muscle.
Observational study in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02920671 (Skeletal Muscle Oxidative Phosphorylation Capacity and Nutrient Homeostasis in Individuals With Primary), which is not on this map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Skeletal Muscle Oxidative Phosphorylation Capacity and Nutrient Homeostasis in Individuals With Primary (Genetic) and Secondary (Obesity-related) Mitochondrial Impairment as Compared to Healthy, Normal-weight Individuals
Who cites it
1 citing paper in PubMed.
- Safety and efficacy of individualised exercise and NADThe Lancet. Neurology · 2026Trial
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
Abstract
introductionFriedreich's ataxia (FRDA) is a multisystem disorder caused by frataxin deficiency. FRDA-related diabetes mellitus (DM) is common. Frataxin supports skeletal muscle mitochondrial oxidative phosphorylation (OXPHOS) capacity, a mediator of insulin sensitivity. Our objective was to test the association between skeletal muscle health and insulin sensitivity and secretion in adults with FRDA without DM.
methodsCase-control study (NCT02920671). Glucose and insulin metabolism (stable-isotope oral glucose tolerance tests), body composition (dual-energy x-ray absorptiometry), physical activity (self-report), and skeletal muscle OXPHOS capacity (creatine chemical exchange saturation transfer magnetic resonance imaging) were assessed.
resultsParticipants included 11 individuals with FRDA (4 female), median age 27 years (interquartile range 23, 39), body mass index 26.9 kg/m2 (24.1, 29.4), and 24 controls (11 female), 29 years (26, 39), 24.4 kg/m2 (21.8, 27.0). Fasting glucose was higher in FRDA [91 vs 83 mg/dL (5.0 vs 4.6 mmol/L), P < .05]. Individuals with FRDA had lower insulin sensitivity (whole-body insulin sensitivity index 2.8 vs 5.3, P < .01), higher postprandial insulin secretion (insulin secretory rate incremental area under the curve 30-180 minutes, 24 652 vs 17,858, P < .05), and more suppressed postprandial endogenous glucose production (-.9% vs 26.9% of fasting endogenous glucose production, P < .05). In regression analyses, lower OXPHOS and inactivity explained some of the difference in insulin sensitivity. More visceral fat contributed to lower insulin sensitivity independent of FRDA. Insulin secretion accounting for sensitivity (disposition index) was not different.
conclusionLower 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.