Sodium acetate protects against nicotine-induced excess hepatic lipid in male rats by suppressing xanthine oxidase activity

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dc.contributor.authorDangana, Elizabeth
dc.contributor.authorOmolekulo, Tolulope
dc.contributor.authorAreola, Emmanuel
dc.contributor.authorOlaniyi, Kehinde
dc.contributor.authorSoladoye, Ayodele
dc.contributor.authorOlatunji, Lawrence Aderemi
dc.date.accessioned2025-05-08T11:19:36Z
dc.date.available2025-05-08T11:19:36Z
dc.date.issued2019-12-15
dc.description.abstractFatty liver is the hepatic consequence of chronic insulin resistance (IR) and related syndromes. It is mostly accompanied by inflammatory and oxidative molecules. Increased activity of xanthine oxidase (XO) exerts both inflammatory and oxidative effects and has been implicated in metabolic derangements including non-alcoholic fatty liver disease. Short chain fatty acids (SCFAs) elicit beneficial metabolic alterations in IR and related syn dromes. In the present study, we evaluated the preventive effects of a SCFA, acetate, on nicotine-induced dys metabolism and fatty liver. Twenty-four male Wistar rats (n = 6/group): vehicle-treatment (p.o.), nicotine treated (1.0 mg/kg; p.o.), sodium acetate-treated (200 mg/kg; p.o.) and nicotine + sodium acetate-treated groups. The treatments lasted for 8 weeks. IR was estimated by oral glucose tolerance test and homeostatic model assessment of IR. Plasma and hepatic free fatty acid, triglyceride (TG), glutathione peroxidase, adenosine deaminase (ADA), XO and uric acid (UA) were measured. Nicotine exposure resulted in reduced body weight, liver weight, visceral adiposity, glycogen content and glycogen synthase activity. Conversely, exposure to ni cotine increased fasting plasma glucose, lactate, IR, plasma and hepatic TG, free fatty acid, TG/HDL-cholesterol ratio, lipid peroxidation, liver function enzymes, plasma and hepatic UA, XO and ADA activities. However, plasma and hepatic glucose-6-phosphate dehydrogenase-dependent antioxidant defense was not affected by nicotine. Concomitant treatment with acetate ameliorated nicotine-induced effects. Taken together, these results indicate that nicotine exposure leads to excess deposition of lipid in the liver by enhancing XO activity. The results also imply that acetate confers hepatoprotection and is accompanied by decreased XO activity.
dc.description.sponsorshipThere was no funding for this research work
dc.identifier.citationDangana, E.O., Omolekulo, T.E., Areola E.D., Olaniyi, K.S., Soladoye, A.O., & Olatunji, L.A. (2020). Sodium acetate protects against nicotine-induced excess hepatic lipid in male rats by suppressing xanthine oxidase activity. Chemico-Biological Interactions, 316, 108929, Published by Elsevier. Available online at: Chemico-Biological Interactions | Vol 316, 25 January 2020 | ScienceDirect.com by Elsevier
dc.identifier.uri10.1016/j.cbi.2019.108929
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/16430
dc.language.isoen
dc.publisherElsevier
dc.relation.ispartofseries316; 108929
dc.subjectShort-chain fatty acid
dc.subjectXanthine oxidase
dc.subjectFatty liver
dc.subjectNicotine
dc.subjectAcetate
dc.titleSodium acetate protects against nicotine-induced excess hepatic lipid in male rats by suppressing xanthine oxidase activity
dc.typeArticle

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