Sodium acetate protects against nicotine-induced excess hepatic lipid in male rats by suppressing xanthine oxidase activity
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Date
2019-12-15
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Publisher
Elsevier
Abstract
Fatty 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.
Description
Keywords
Short-chain fatty acid, Xanthine oxidase, Fatty liver, Nicotine, Acetate
Citation
Dangana, 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