ArticleMetabolites2025
NAD
Article in Metabolites, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
2 authors.
Funding
Abstract
BACKGROUND/
objectivesStimulation of glucose uptake in response to ischemic stress is important for cardiomyocyte post-ischemic function and survival. In the diabetic myocardium chronically exposed to an excess of circulating lipids, this mechanism is impaired, making the myocardium more sensitive to ischemia-reperfusion injury (IRI). In vitro studies have shown that exposure to fatty acids (FAs) reduces basal and stimulated glucose uptake in cardiomyocytes. Preliminary results indicate reduced NAD
methodsPrimary rat cardiomyocytes were chronically treated with the sirtuin deacetylase inhibitor nicotinamide (NAM) in absence of FAs to induce protein acetylation. Conversely, we replenished NAD
resultsSimilar to FA exposure, NAM treatment increased protein acetylation and impaired metabolic-stress-stimulated glucose uptake in cardiomyocytes. In contrast, NR supplementation reduced protein acetylation and improved metabolic-stress-stimulated glucose uptake in FA-exposed cardiomyocytes. Neither NAM nor NR influenced insulin-stimulated glucose uptake. Both NAM and FAs induced hydroxyacyl-CoA dehydrogenase trifunctional enzyme subunit α (HADHA) acetylation on lysine residues K
conclusionsIn cardiomyocytes, protein hyperacetylation, resulting from either FA exposure or sirtuin inhibition, impairs metabolic-stress-stimulated glucose uptake and is associated with increased FA oxidation.
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