ArticleDiabetologia2018
Impact of prolonged overfeeding on skeletal muscle mitochondria in healthy individuals.
Article in Diabetologia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01672632 (Fat Cell Size and Overfeeding and Etopic Study), which is not on this map. Cited by 12 papers.
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.
Fat Cell Size and Overfeeding and Etopic Study
Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Prediabetes Associates With Musculoskeletal Alterations Independent of Total Body Adiposity.Journal of cachexia, sarcopenia and muscle · 2026Article
- The Hidden Price of Plenty: Oxidative Stress and Calorie-Induced Cardiometabolic Dysfunction.Life (Basel, Switzerland) · 2025Review
- Mitochondrial Dysfunction and Risk Factors for Noncommunicable Diseases: From Basic Concepts to Future Prospective.Diseases (Basel, Switzerland) · 2024Review
- Molecular mechanisms of lipid droplets-mitochondria coupling in obesity and metabolic syndrome: insights and pharmacological implications.Frontiers in physiology · 2024Review
- Nonequilibrium thermodynamics and mitochondrial protein content predict insulin sensitivity and fuel selection during exercise in human skeletal muscle.Frontiers in physiology · 2023Article
- Insulin and IGF-1 receptors regulate complex I-dependent mitochondrial bioenergetics and supercomplexes via FoxOs in muscle.The Journal of clinical investigation · 2021Article
- Impact of moderate exercise on fatty acid oxidation in pancreatic β-cells and skeletal muscle.Journal of endocrinological investigation · 2021Review
- Transcriptomic Regulation of Muscle Mitochondria and Calcium Signaling by Insulin/IGF-1 Receptors Depends on FoxO Transcription Factors.Frontiers in physiology · 2021Article
- Are Alterations in Skeletal Muscle Mitochondria a Cause or Consequence of Insulin Resistance?International journal of molecular sciences · 2020Review
- Human skeletal muscle metabolic responses to 6 days of high-fat overfeeding are associated with dietary n-3PUFA content and muscle oxidative capacity.Physiological reports · 2020Article
- Dynamic changes of muscle insulin sensitivity after metabolic surgery.Nature communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
aims/hypothesesReduced mitochondrial capacity in skeletal muscle has been observed in obesity and type 2 diabetes. In humans, the aetiology of this abnormality is not well understood but the possibility that it is secondary to the stress of nutrient overload has been suggested. To test this hypothesis, we examined whether sustained overfeeding decreases skeletal muscle mitochondrial content or impairs function.
methodsTwenty-six healthy volunteers (21 men, 5 women, age 25.3 ± 4.5 years, BMI 25.5 ± 2.4 kg/m
resultsWith overfeeding, volunteers gained 7.7 ± 1.8 kg (% change 9.8 ± 2.3). Overfeeding increased fasting NEFA, LDL-cholesterol and insulin concentrations. Indirect calorimetry showed a shift towards greater reliance on lipid oxidation. In skeletal muscle tissue, overfeeding increased ceramide content, lipid droplet content and perilipin-2 mRNA expression. Phosphorylation of AMP-activated protein kinase was decreased. Overfeeding increased mRNA expression of certain genes coding for mitochondrial proteins (CS, OGDH, CPT1B, UCP3, ANT1). Despite the stress of nutrient overload, mitochondrial content and mitochondrial respiration in muscle did not change after overfeeding. Similarly, overfeeding had no effect on either the emission of reactive oxygen species or on mitochondrial function in vivo. CONCLUSIONS/
interpretationSkeletal muscle mitochondria are significantly resilient to nutrient overload. The lower skeletal muscle mitochondrial oxidative capacity in human obesity is likely to be caused by reasons other than nutrient overload per se.
trial registrationClinicalTrials.gov NCT01672632.
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Registered trials
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