ReviewJournal of inherited metabolic disease2010
Pathophysiology of fatty acid oxidation disorders.
Review in Journal of inherited metabolic disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 63 citations in OpenAlex.
- Diagnostic challenges and outcome of fatty acid oxidation defects in a tertiary care center in Lebanon.Orphanet journal of rare diseases · 2024Article
- Medium-chain Acyl-COA dehydrogenase deficiency: Pathogenesis, diagnosis, and treatment.Endocrinology, diabetes & metabolism · 2023Review
- Evidence that Oxidative Disbalance and Mitochondrial Dysfunction are Involved in the Pathophysiology of Fatty Acid Oxidation Disorders.Cellular and molecular neurobiology · 2022Review
- Diagnosis and Management of Inborn Errors of Metabolism in Adult Patients in the Emergency Department.Diagnostics (Basel, Switzerland) · 2021Review
- Biochemical Markers for the Diagnosis of Mitochondrial Fatty Acid Oxidation Diseases.Journal of clinical medicine · 2021Review
- Transcriptome analysis suggests a compensatory role of the cofactors coenzyme A and NADScientific reports · 2019Article
- Health services use among children diagnosed with medium-chain acyl-CoA dehydrogenase deficiency through newborn screening: a cohort study in Ontario, Canada.Orphanet journal of rare diseases · 2019Article
- Open-label clinical trial of bezafibrate treatment in patients with fatty acid oxidation disorders in Japan.Molecular genetics and metabolism reports · 2018Article
- Infant with hepatomegaly and hypoglycemia: A setting for fatty acid oxidation defects.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2017Article
- Short-chain acyl-CoA dehydrogenase deficiency: from gene to cell pathology and possible disease mechanisms.Journal of inherited metabolic disease · 2017Review
- Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency.Metabolic brain disease · 2017Article
- Hypoinsulinaemic, hypoketotic hypoglycaemia due to mosaic genetic activation of PI3-kinase.European journal of endocrinology · 2017Article
- Living on the edge: substrate competition explains loss of robustness in mitochondrial fatty-acid oxidation disorders.BMC biology · 2016Article
- Bidirectional Relationships and Disconnects between NAFLD and Features of the Metabolic Syndrome.International journal of molecular sciences · 2016Review
- Mitochondrial dysfunction in fatty acid oxidation disorders: insights from human and animal studies.Bioscience reports · 2015Review
- Rhabdomyolysis-Associated Mutations in Human LPIN1 Lead to Loss of Phosphatidic Acid Phosphohydrolase Activity.JIMD reports · 2015Article
- Dietary fat and antioxidant vitamin intake in patients of neurodegenerative disease in a rural region of Jalisco, Mexico.Nutritional neuroscience · 2014Article
- High grade glioblastoma is associated with aberrant expression of ZFP57, a protein involved in gene imprinting, and of CPT1A and CPT1C that regulate fatty acid metabolism.Cancer biology & therapy · 2014Article
- Rodent models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.International journal of molecular sciences · 2013Review
- Evaluation of the child with suspected mitochondrial liver disease.Journal of pediatric gastroenterology and nutrition · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial fatty acid oxidation represents an important pathway for energy generation during periods of increased energy demand such as fasting, febrile illness and muscular exertion. In liver, the primary end products of the pathway are ketone bodies, which are released into the circulation and provide energy to tissues that are not able to oxidize fatty acids such as brain. Other tissues, such as cardiac and skeletal muscle are capable of direct utilization of the fatty acids as sources of energy. This article provides an overview of the pathogenesis of fatty acid oxidation disorders. It describes the different tissue involvement with the disease processes and correlates disease phenotype with the nature of the genetic defect for the known disorders of the pathway.
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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.