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 syndromes. In the present study, we evaluated the preventive effects of a SCFA, acetate, on nicotine-induced dysmetabolism 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 nicotine 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.

中文翻译：

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乙酸钠可通过抑制黄嘌呤氧化酶的活性来防止尼古丁引起的雄性大鼠肝脂质过多。

脂肪肝是慢性胰岛素抵抗（IR）和相关综合征的肝脏后果。它主要伴有炎性和氧化性分子。黄嘌呤氧化酶（XO）活性的增强同时发挥了炎症和氧化作用，并与包括非酒精性脂肪肝在内的代谢紊乱有关。短链脂肪酸（SCFA）在IR和相关综合症中引起有益的代谢改变。在本研究中，我们评估了SCFA，乙酸盐对尼古丁引起的代谢不良和脂肪肝的预防作用。24只雄性Wistar大鼠（n = 6 /组）：媒介物处理（po），尼古丁处理（1.0 mg / kg; po），醋酸钠处理（200 mg / kg; po）和尼古丁+乙酸钠治疗组。治疗持续了8周。IR是通过口服葡萄糖耐量试验和IR的稳态模型评估来估计的。测量血浆和肝游离脂肪酸，甘油三酸酯（TG），谷胱甘肽过氧化物酶，腺苷脱氨酶（ADA），XO和尿酸（UA）。尼古丁暴露导致体重，肝脏重量，内脏脂肪，糖原含量和糖原合酶活性降低。相反，暴露于尼古丁会增加空腹血糖，乳酸，IR，血浆和肝TG，游离脂肪酸，TG / HDL-胆固醇比，脂质过氧化，肝功能酶，血浆和肝UA，XO和ADA活性。然而，血浆和肝葡萄糖6-磷酸脱氢酶依赖性抗氧化防御不受烟碱的影响。醋酸盐的伴随治疗改善了尼古丁引起的作用。在一起 这些结果表明，尼古丁的暴露通过增强XO活性导致肝脏中脂质的过多沉积。结果还暗示乙酸盐赋予肝保护作用，并伴有XO活性降低。