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Allopurinol and valproic acid improve cardiac triglyceride and Na+-K+-ATPase activity independent of circulating aldosterone in female rats with glucose intolerance

dc.contributor.authorTolulope E. Adegoke, Isiah W. Sabinari, Taofeek O. Usman, Toyyib O. Abdulkareem, Olugbenga S. Michael, Oluwaseun A. Adeyanju, Chinaza Dibia, Omotola O. Omotoye, Adewumi O. Oyabambi & Lawrence A. Olatunji
dc.date.accessioned2026-04-18T17:35:41Z
dc.date.available2026-04-18T17:35:41Z
dc.date.issued2020
dc.description.abstractContext: Studies have shown that cardiac triglyceride accumulation and impaired Naþ-Kþ-ATPase activity are linked to diabetes- related cardiovascular disease, particularly in women. Objectives: We hypothesised that allopurinol (ALL) and valproic acid (VPA) treatment would improve cardiac triglyceride and Naþ-Kþ-ATPase activity independent of circulating aldosterone in Combined Oral Contraceptive (COC)-induced dysglycemia Materials and methods: Rats received COC (1.0 lg ethinylestradiol and 5.0 lg levonorgestrel; po) with or without ALL (1 mg; po) and VPA (20mg; po) for 6weeks. Results: COC-treatment led to impaired glucose tolerance, accumulated abdominal fat, dyslipidemia, elevated plasma MDA, PAI-1 and aldosterone levels and also reduced plasma nitric oxide bioavailability and cardiac Naþ-Kþ-ATPase activity. However, either ALL or VPA treatment ameliorated these alterations comparably independent of elevated aldosterone level Discussion and conclusion: Our results suggest that either ALL or VPA would improve cardiac TG and Naþ-Kþ-ATPase activity comparably in COC-treated rats, regardless of circulating aldosterone level.
dc.identifier.citation8
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/17366
dc.language.isoen
dc.publisherTaylor & Francis
dc.subjectCardiac Naþ-Kþ-ATPase
dc.subjectcardiometabolic syndrome
dc.subjecttriglyceride
dc.subjecthyperinsulinemia
dc.subjecthypeuricaemia
dc.titleAllopurinol and valproic acid improve cardiac triglyceride and Na+-K+-ATPase activity independent of circulating aldosterone in female rats with glucose intolerance
dc.typeArticle

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