ArticleDiabetes2015
Rapid Repression of ADP Transport by Palmitoyl-CoA Is Attenuated by Exercise Training in Humans: A Potential Mechanism to Decrease Oxidative Stress and Improve Skeletal Muscle Insulin Signaling.
Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Carbohydrate restriction drives greater perturbations in circulating metabolites than low energy availability in elite male athletes.Physiological reports · 2026Trial
- Reducing the mitochondrial oxidative burden alleviates lipid-induced muscle insulin resistance in humans.Science advances · 2024Article
- Mitochondrial bioenergetics are not associated with myofibrillar protein synthesis rates.Journal of cachexia, sarcopenia and muscle · 2024Article
- Direct and indirect targets of carboxyatractyloside, including overlooked toxicity toward nucleoside diphosphate kinase (NDPK) and mitochondrial HPharmaceutical biology · 2023Review
- Insights into the development of insulin resistance: Unraveling the interaction of physical inactivity, lipid metabolism and mitochondrial biology.Frontiers in physiology · 2023Review
- The Mitochondrial Protein MitoNEET as a Probe for the Allostery of Glutamate Dehydrogenase.Molecules (Basel, Switzerland) · 2022Article
- Oxidative phosphorylation KBiochimica et biophysica acta. Bioenergetics · 2021Article
- Are Alterations in Skeletal Muscle Mitochondria a Cause or Consequence of Insulin Resistance?International journal of molecular sciences · 2020Review
- Acute insulin deprivation results in altered mitochondrial substrate sensitivity conducive to greater fatty acid transport.American journal of physiology. Endocrinology and metabolism · 2020Article
- Reactive oxygen species-dependent regulation of pyruvate dehydrogenase kinase-4 in white adipose tissue.American journal of physiology. Cell physiology · 2020Article
- Adipose Tissue Inflammation Is Directly Linked to Obesity-Induced Insulin Resistance, while Gut Dysbiosis and Mitochondrial Dysfunction Are Not Required.Function (Oxford, England) · 2020Article
- Quantification of Mitochondrial Oxidative Phosphorylation in Metabolic Disease: Application to Type 2 Diabetes.International journal of molecular sciences · 2019Review
- Sex differences in mitochondrial respiratory function in human skeletal muscle.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Dominant and sensitive control of oxidative flux by the ATP-ADP carrier in human skeletal muscle mitochondria: Effect of lysine acetylation.Archives of biochemistry and biophysics · 2018Article
- Blood lactate accumulation decreases during the slow component of oxygen uptake without a decrease in muscular efficiency.Pflugers Archiv : European journal of physiology · 2017Article
- Nutrition and Training Influences on the Regulation of Mitochondrial Adenosine Diphosphate Sensitivity and Bioenergetics.Sports medicine (Auckland, N.Z.) · 2017Review
- Skeletal muscle mitochondria as a target to prevent or treat type 2 diabetes mellitus.Nature reviews. Endocrinology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondrial ADP transport may represent a convergence point unifying two prominent working models for the development of insulin resistance, as reactive lipids (specifically palmitoyl-CoA [P-CoA]) can inhibit ADP transport and subsequently increase mitochondrial reactive oxygen species emissions. In the current study, we aimed to determine if exercise training in humans diminished P-CoA attenuation of mitochondrial ADP respiratory sensitivity. Six weeks of exercise training increased whole-body glucose homeostasis and skeletal muscle Akt signaling and reduced markers of oxidative stress without reducing maximal mitochondrial H2O2 emissions. To ascertain if enhanced mitochondrial ADP transport contributed to the improvement in the in vivo oxidative state, we determined mitochondrial ADP sensitivity in the presence and absence of P-CoA. In the absence of P-CoA, exercise training reduced mitochondrial ADP sensitivity. In contrast, exercise training increased mitochondrial ADP sensitivity with P-CoA present. We further show that P-CoA noncompetitively inhibits mitochondrial ADP transport and the ability of ADP to attenuate mitochondrial H2O2 emission. Altogether, the current data provide a potential mechanism for how P-CoA contributes to insulin resistance and highlight the ability of exercise training to diminish P-CoA attenuation in mitochondrial ADP transport.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.