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Functional hypoxia is a stress condition caused by the abalone itself as a result of increased muscle activity, which generally necessitates the employment of anaerobic metabolism if the activity is sustained for prolonged periods. With that being said, abalone are highly reliant on anaerobic metabolism to provide partial compensation for energy production during oxygen-deprived episodes. However, current knowledge on the holistic metabolic response for energy metabolism during functional hypoxia, and the contribution of different metabolic pathways and various abalone tissues towards the overall accumulation of anaerobic end-products in abalone are scarce. Metabolomics analysis of adductor muscle, foot muscle, left gill, right gill, haemolymph and epipodial tissue samples indicated that South African abalone ( subjected to functional hypoxia utilises predominantly anaerobic metabolism, and depends on all of the main metabolite classes (proteins, carbohydrates and lipids) for energy supply. Functional hypoxia caused increased levels of anaerobic end-products: lactate, alanopine, tauropine, succinate and alanine. Also, elevation in arginine levels was detected, confirming that abalone use phosphoarginine to generate energy during functional hypoxia. Different tissues showed varied metabolic responses to hypoxia, with functional hypoxia showing excessive changes in the adductor muscle and gills. From this metabolomics investigation, it becomes evident that abalone are metabolically able to produce sufficient amounts of energy when functional hypoxia is experienced. Also, tissue interplay enables the adjustment of energy requirements as their metabolism shifts from aerobic to anaerobic respiration during functional hypoxia.This article has an associated First Person interview with the first author of the paper.
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http://dx.doi.org/10.1242/bio.031070 | DOI Listing |
Liver Int
October 2025
Division of Gastroenterology, Acireale Hospital, Azienda Sanitaria Provinciale di Catania, Catania, Italy.
Background And Aims: Gut-liver axis has been implicated in the pathophysiology of cirrhosis due to metabolic dysfunction-associated steatotic liver disease (MASLD), an in vitro model for studying epithelial gut dysfunction in MASLD is lacking. In this study, we aimed to characterise intestinal organoids derived from subjects with MASLD.
Materials And Methods: Intestinal organoids were obtained from duodenal samples of individuals with non-fibrotic MASLD and with MASLD-cirrhosis.
J Biomed Sci
September 2025
Division of Gastroenterology, Department of Medicine, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Oncometabolites are aberrant metabolic byproducts that arise from mutations in enzymes of the tricarboxylic acid (TCA) cycle or related metabolic pathways and play central roles in tumor progression and immune evasion. Among these, 2-hydroxyglutarate (2-HG), succinate, and fumarate are the most well-characterized, acting as competitive inhibitors of α-ketoglutarate-dependent dioxygenases to alter DNA and histone methylation, cellular differentiation, and hypoxia signaling. More recently, itaconate, an immunometabolite predominantly produced by activated macrophages, has been recognized for its dual roles in modulating inflammation and tumor immunity.
View Article and Find Full Text PDFRespir Physiol Neurobiol
September 2025
Department of Pediatrics, School of Medicine, Duke University.
Pompe disease is an autosomal recessive neuromuscular disorder characterized by a deficiency of acid α-glucosidase (GAA), an enzyme responsible for lysosomal glycogen degradation in all cells. Respiratory distress is a common symptom among patients with Pompe disease resulting from weakness of primary respiratory neuromuscular units of the diaphragm and genioglossus and the motor neurons which innervate them. The only FDA approved treatment is enzyme replacement therapy (ERT) of recombinant human GAA (rhGAA) which slows the decline of motor function and extends life expectancy.
View Article and Find Full Text PDFGene
September 2025
Institute of Physiology, Medical School, University of Pécs H-7624 Pécs, Hungary. Electronic address:
In this edition of Gene's "Editor's Corner" we summarize the complex interactions of different molecular mechanisms behind the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). The topic is relevant, as the therapeutic options for HIE are limited, it is important to have as much knowledge as possible about the molecular processes underlying the disease. In the recent issue of Gene (Gene 952, 2025, 149363), Wang et al.
View Article and Find Full Text PDFJ Neurophysiol
September 2025
Department of Radiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang 110004, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a significant cause of developmental disorders and permanent central nervous system damage, with functional recovery closely linked to myelin sheath integrity. This study aimed to analyze the expression of pH and the voltage-gated proton channel (Hv1) in the brains of neonatal pigs with HIE at various time points, alongside changes in myelin-related proteins. MRI was employed to localize the basal ganglia and assess pH changes post-hypoxia-ischemia, while immunofluorescence staining was used to evaluate Hv1, myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), and myelin-associated glycoprotein (MAG).
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