ArticleProceedings of the National Academy of Sciences of the United States of America2007
Reduced expression of mitochondrial frataxin in mice exacerbates diet-induced obesity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 36 citations in OpenAlex.
- Longitudinal analysis of anthropometric measures over 5 years in patients with Friedreich ataxia in the EFACTS natural history study.European journal of neurology · 2025Article
- Frataxin Loss Promotes Angiotensin II-Induced Endothelial-to-Mesenchymal Transition.Journal of the American Heart Association · 2024Article
- The crosstalk between mitochondrial quality control and metal-dependent cell death.Cell death & disease · 2024Review
- Butyrate prevents visceral adipose tissue inflammation and metabolic alterations in a Friedreich's ataxia mouse model.iScience · 2023Article
- Iron Metabolism in Obesity and Metabolic Syndrome.International journal of molecular sciences · 2020Review
- The vital role of ATP citrate lyase in chronic diseases.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Impairment of insulin signalling in peripheral tissue fails to extend murine lifespan.Aging cell · 2017Article
- Obesity: considerations about etiology, metabolism, and the use of experimental models.Diabetes, metabolic syndrome and obesity : targets and therapy · 2012Article
- A gene expression phenotype in lymphocytes from Friedreich ataxia patients.Annals of neurology · 2011Article
- Article
- Opposing effects of dietary sugar and saturated fat on cardiovascular risk factors and glucose metabolism in mitochondrially impaired mice.European journal of nutrition · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Published evidence suggests that adiposity in humans may be linked to impaired energy expenditure for reasons widely unresolved. We have generated mice with a systemic impairment of oxidative phosphorylation (OXPHOS) due to aP2 cre-mediated targeted disruption, and unexpectedly ubiquitous reduction of mitochondrial frataxin protein expression. Only when maintained on a high-calorie diet resembling Westernized eating habits, these animals accumulate additional body fat, leading to increased body mass, and develop diabetes mellitus, despite the fact that both calorie uptake and physical activity were identical to that in control animals. This phenotype is caused by a mild but significant reduction in total energy expenditure paralleled by increased expression of ATP citrate lyase, a rate-limiting step in de novo synthesis of fatty acids and triglycerides. Taken together, these findings indicate that a limited impairment in oxidative metabolism within the mitochondria directly predisposes mammals to excessive body weight gain.
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.