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10.1038/s42003-025-09149-7 http://scihub22266oqcxt.onion/10.1038/s42003-025-09149-7 41381852!12698834!41381852     free     free     free       Commun+Biol 2025 ; 8 (1): 1759 Nephropedia Template TP {{tp|p=41381852|t=2025. Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency |pdf=|usr=}}{{41381852}} gab.com Text Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency JO: Commun Biol http://www.kidney.de/pget.php?&tw=1&pmid=41381852 #FOAvip Hypermetabolism, a futile cycle of energy production and consumption, has been proposed as an adaptative response to deficiencies in mitochondrial oxidative phosphorylation. However, the cellular costs of hypermetabolism remain largely unknown. Here we studied the consequences of hypermetabolism in human motor neurons harboring a heteroplasmic mutation in MT-ATP6, which impairs ATP synthase assembly. Respirometry, metabolomics, and proteomics analyses of the motor neurons showed that elevated ATP production rates were accompanied with increased demand for acetyl-Coenzyme A (acetyl-CoA) and depleted pantothenate (vitamin B5), and the proteome was remodeled to support the metabolic adaptation. Mitochondrial membrane potential and coupling efficiency remained stable, and the therapeutic agent avanafil did not affect metabolite levels. However, a redistribution of acetyl-CoA usage resulted in metabolic trade-offs, including reduced histone acetylation and altered maintenance of the neurotransmitter acetylcholine, revealing potential vulnerabilities in motor neurons. These findings advance the understanding of cellular metabolic consequences imposed by hypermetabolic conditions. Twit Text FOAVip Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency ????Commun Biol http://www.kidney.de/pget.php?&tw=1&pmid=41381852 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41381852 #FOAvip English Wikipedia <ref>{{Cite pmid|41381852}}</ref> Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency #MMPMID41381852 Torregrosa-Munumer R; Turkia J; Ermis R; Kvist J; Harjuhaahto S; Pennonen J; Hietakangas V; Ylikallio E; Tyynismaa H Commun Biol 2025[Dec]; 8 (1): 1759 PMID41381852show ga Hypermetabolism, a futile cycle of energy production and consumption, has been proposed as an adaptative response to deficiencies in mitochondrial oxidative phosphorylation. However, the cellular costs of hypermetabolism remain largely unknown. Here we studied the consequences of hypermetabolism in human motor neurons harboring a heteroplasmic mutation in MT-ATP6, which impairs ATP synthase assembly. Respirometry, metabolomics, and proteomics analyses of the motor neurons showed that elevated ATP production rates were accompanied with increased demand for acetyl-Coenzyme A (acetyl-CoA) and depleted pantothenate (vitamin B5), and the proteome was remodeled to support the metabolic adaptation. Mitochondrial membrane potential and coupling efficiency remained stable, and the therapeutic agent avanafil did not affect metabolite levels. However, a redistribution of acetyl-CoA usage resulted in metabolic trade-offs, including reduced histone acetylation and altered maintenance of the neurotransmitter acetylcholine, revealing potential vulnerabilities in motor neurons. These findings advance the understanding of cellular metabolic consequences imposed by hypermetabolic conditions. |*Energy Metabolism[MESH] |*Mitochondrial Proton-Translocating ATPases/deficiency/genetics/metabolism[MESH] |*Motor Neurons/metabolism[MESH] |Acetyl Coenzyme A/metabolism[MESH] |Adenosine Triphosphate/metabolism[MESH] |Humans[MESH]Metabolic costs and trade-offs of hypermetabolism in human motor neuro(epmc).pdf DeepDyve Pubget Overpricing