ArticleAmino acids2016
Creatine transporter deficiency leads to increased whole body and cellular metabolism.
Article in Amino acids, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 44 citations in OpenAlex.
- The skeletal muscle-adipose creatine metabolic axis: A novel paradigm for lipid metabolism reprogramming and obesity management.Experimental physiology · 2026Review
- Effects of SLC6A8 mutation-induced creatine deficiency on cellular function in fibroblasts.Scientific reports · 2025Article
- Creatine transporter (SLC6A8) knockout mice exhibit reduced muscle performance, disrupted mitochondrial CaCell death & disease · 2025Article
- Intratesticular creatine maintains spermatogenesis by defining tight junctions.Scientific reports · 2024Article
- A Gad2 specific Slc6a8 deletion recapitulates the contextual and cued freezing deficits seen in Slc6a8Brain research · 2024Article
- Therapeutic outcome of patients with Lennox-Gastaut syndrome with mitochondrial respiratory chain complex I deficiency.Frontiers in neurology · 2024Article
- Cell-specific vulnerability to metabolic failure: the crucial role of parvalbumin expressing neurons in creatine transporter deficiency.Acta neuropathologica communications · 2023Article
- Creatine transporter-deficient rat model shows motor dysfunction, cerebellar alterations, and muscle creatine deficiency without muscle atrophy.Journal of inherited metabolic disease · 2022Article
- Review
- Thermogenic Fat: Development, Physiological Function, and Therapeutic Potential.International journal of molecular sciences · 2021Review
- Current Evidence and Possible Future Applications of Creatine Supplementation for Older Adults.Nutrients · 2021Review
- Creatine metabolism: energy homeostasis, immunity and cancer biology.Nature reviews. Endocrinology · 2020Review
- Opportunities and challenges in the therapeutic activation of human energy expenditure and thermogenesis to manage obesity.The Journal of biological chemistry · 2020Review
- UCP1 Dependent and Independent Thermogenesis in Brown and Beige Adipocytes.Frontiers in endocrinology · 2020Review
- The Creatine Transporter Unfolded: A Knotty Premise in the Cerebral Creatine Deficiency Syndrome.Frontiers in synaptic neuroscience · 2020Review
- Dodecyl creatine ester-loaded nanoemulsion as a promising therapy for creatine transporter deficiency.Nanomedicine (London, England) · 2019Article
- A Nervous System-Specific Model of Creatine Transporter Deficiency Recapitulates the Cognitive Endophenotype of the Disease: a Longitudinal Study.Scientific reports · 2019Article
- Cognitive deficits and increases in creatine precursors in a brain-specific knockout of the creatine transporter gene Slc6a8.Genes, brain, and behavior · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Creatine (Cr) is a guanidino compound required for rapid replenishment of ATP in cells with a high-energy demand. In humans, mutations in the Cr transporter (CRT;SLC6A8) prevent Cr entry into tissue and result in a significant intellectual impairment, epilepsy, and aphasia. The lack of Cr on both the whole body and cellular metabolism was evaluated in Crt knockout (Crt (-/y) ) mice, a high-fidelity model of human CRT deficiency. Crt (-/y) mice have reduced body mass and, however, show a twofold increase in body fat. There was increased energy expenditure in a home cage environment and during treadmill running in Crt (-/y) mice. Consistent with the increases in the whole-body metabolic function, Crt (-/y) mice show increased cellular metabolism as well. Mitochondrial respiration increased in skeletal muscle fibers and hippocampal lysates from Crt (-/y) mice. In addition, Crt (-/y) mice had increased citrate synthase activity, suggesting a higher number of mitochondria instead of an increase in mitochondrial activity. To determine if the increase in respiration was due to increased mitochondrial numbers, we measured oxygen consumption in an equal number of mitochondria from Crt (+/y) and Crt (-/y) mice. There were no changes in mitochondrial respiration when normalized to mitochondrial number, suggesting that the increase in respiration observed could be to higher mitochondrial content in Crt (-/y) mice.
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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.