ArticleThe Journal of clinical endocrinology and metabolism2012
Mitochondrial oxidative phosphorylation is impaired in patients with congenital lipodystrophy.
Article in The Journal of clinical endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- Metabolic Dysregulation in Laminopathies: Implications for Heart Failure and Cardiac Health.Current heart failure reports · 2026Review
- Skeletal MuscleJournal of cachexia, sarcopenia and muscle · 2025Article
- Mitochondrial Dysfunction Correlates with Brain Amyloid Binding, Memory, and Executive Function in Down Syndrome: Implications for Alzheimer's Disease in Down Syndrome.Brain sciences · 2025Article
- Discovering cellular programs of intrinsic and extrinsic drivers of metabolic traits using LipocyteProfiler.Cell genomics · 2023Article
- Impaired Muscle Mitochondrial Function in Familial Partial Lipodystrophy.The Journal of clinical endocrinology and metabolism · 2022Observational
- Metabolomic Analysis of the Effects of Leptin Replacement Therapy in Patients with Lipodystrophy.Journal of the Endocrine Society · 2020Article
- Accumulation of saturated intramyocellular lipid is associated with insulin resistance.Journal of lipid research · 2019Article
- Differences in Muscle Metabolism Between Triathletes and Normally Active Volunteers Investigated Using Multinuclear Magnetic Resonance Spectroscopy at 7T.Frontiers in physiology · 2018Article
- In-vivoAnalytical biochemistry · 2017Review
- Spatially localized phosphorous metabolism of skeletal muscle in Duchenne muscular dystrophy patients: 24-month follow-up.PloS one · 2017Article
- Skeletal muscle alkaline Pi pool is decreased in overweight-to-obese sedentary subjects and relates to mitochondrial capacity and phosphodiester content.Scientific reports · 2016Article
- Lipodystrophic diabetes mellitus: a lesson for other forms of diabetes?Current diabetes reports · 2015Review
- Insulin resistance is associated with epigenetic and genetic regulation of mitochondrial DNA in obese humans.Clinical epigenetics · 2015Article
- Postexercise phosphocreatine recovery, an index of mitochondrial oxidative phosphorylation, is reduced in diabetic patients with lower extremity complications.Journal of vascular surgery · 2013Article
- What do magnetic resonance-based measurements of Pi→ATP flux tell us about skeletal muscle metabolism?Diabetes · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
objectiveLipid accumulation in skeletal muscle and the liver is strongly implicated in the development of insulin resistance and type 2 diabetes, but the mechanisms underpinning fat accrual in these sites remain incompletely understood. Accumulating evidence of muscle mitochondrial dysfunction in insulin-resistant states has fuelled the notion that primary defects in mitochondrial fat oxidation may be a contributory mechanism. The purpose of our study was to determine whether patients with congenital lipodystrophy, a disorder primarily affecting white adipose tissue, manifest impaired mitochondrial oxidative phosphorylation in skeletal muscle. RESEARCH DESIGN AND
methodsMitochondrial oxidative phosphorylation was assessed in quadriceps muscle using 31P-magnetic resonance spectroscopy measurements of phosphocreatine recovery kinetics after a standardized exercise bout in nondiabetic patients with congenital lipodystrophy and in age-, gender-, body mass index-, and fitness-matched controls.
resultsThe phosphocreatine recovery rate constant (k) was significantly lower in patients with congenital lipodystrophy than in healthy controls (P<0.001). This substantial (∼35%) defect in mitochondrial oxidative phosphorylation was not associated with significant changes in basal or sleeping metabolic rates.
conclusionsMuscle mitochondrial oxidative phosphorylation is impaired in patients with congenital lipodystrophy, a paradigmatic example of primary adipose tissue dysfunction. This finding suggests that changes in mitochondrial oxidative phosphorylation in skeletal muscle could, at least in some circumstances, be a secondary consequence of adipose tissue failure. These data corroborate accumulating evidence that mitochondrial dysfunction can be a consequence of insulin-resistant states rather than a primary defect. Nevertheless, impaired mitochondrial fat oxidation is likely to accelerate ectopic fat accumulation and worsen insulin resistance.
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.