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减轻果糖诱导的大鼠非酒精性脂肪肝。

Mitigates Fructose-Induced Non-Alcoholic Fatty Liver in Rats.

机构信息

Department of Internal Medicine, Faculty of Veterinary Medicine, Erciyes University, Kayseri 38280, Turkey.

Department of Internal Medicine, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur 15030, Turkey.

出版信息

Medicina (Kaunas). 2024 Oct 18;60(10):1713. doi: 10.3390/medicina60101713.

DOI:10.3390/medicina60101713
PMID:39459500
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11509347/
Abstract

Non-alcoholic fatty liver disease (NAFLD) is a growing global health concern closely linked to metabolic disorders, including obesity, insulin resistance, and dyslipidemia. Emerging evidence suggests that the gut-liver axis plays a critical role in the pathogenesis of NAFLD, with recent research highlighting the influence of gut microbiota, including fungal species such as Saccharomyces boulardii (). This study aimed to evaluate the effects of on lipid metabolism and oxidative stress in a rat model of fructose-induced NAFLD. Thirty Wistar rats were divided into three groups: a control group, a fatty liver group induced by 35% fructose supplementation, and a treatment group receiving (100 mg/kg/day) after fructose induction. Biochemical analyses revealed that the treatment group exhibited significantly lower plasma levels of malondialdehyde (MDA), alanine aminotransferase (ALT), total triglycerides, and cholesterol compared to the untreated fatty liver group ( < 0.05). Furthermore, liver tissue analysis showed a marked reduction in lipid accumulation and fatty infiltration in the treatment group, with no visible lipid vacuoles in hepatocytes. The expression of aquaporin-8 (AQP8) and sirtuin-1 (SIRT1), key markers associated with hepatocyte function and lipid metabolism, was significantly higher in the group compared to the fatty liver group ( < 0.001). These findings indicate that supplementation mitigates the metabolic and oxidative stress-related alterations associated with fructose-induced NAFLD. In conclusion, our study suggests that exerts protective effects on the liver by reducing lipid accumulation and oxidative stress, highlighting its potential as a therapeutic intervention for NAFLD.

摘要

非酒精性脂肪性肝病 (NAFLD) 是一个日益严重的全球健康问题,与代谢紊乱密切相关,包括肥胖、胰岛素抵抗和血脂异常。新出现的证据表明,肠道-肝脏轴在 NAFLD 的发病机制中起着关键作用,最近的研究强调了肠道微生物群的影响,包括真菌物种如酿酒酵母(Saccharomyces boulardii ())。本研究旨在评估在果糖诱导的 NAFLD 大鼠模型中对脂质代谢和氧化应激的影响。

将 30 只 Wistar 大鼠分为三组:对照组、35%果糖补充诱导的脂肪肝组和果糖诱导后给予 ()(100mg/kg/天)治疗组。生化分析显示,与未治疗的脂肪肝组相比,治疗组的血浆丙二醛 (MDA)、丙氨酸氨基转移酶 (ALT)、总甘油三酯和胆固醇水平显著降低(<0.05)。此外,肝组织分析显示治疗组的脂质积累和脂肪浸润明显减少,肝细胞中没有可见的脂质空泡。水通道蛋白-8 (AQP8) 和沉默调节蛋白-1 (SIRT1) 的表达在治疗组中明显高于脂肪肝组(<0.001),这两种蛋白都是与肝细胞功能和脂质代谢相关的关键标志物。

这些发现表明补充 () 减轻了与果糖诱导的 NAFLD 相关的代谢和氧化应激相关的改变。总之,我们的研究表明,通过减少脂质积累和氧化应激,对肝脏发挥保护作用,强调了其作为 NAFLD 治疗干预的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32cc/11509347/fd7f6f51d59d/medicina-60-01713-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32cc/11509347/fd7f6f51d59d/medicina-60-01713-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/32cc/11509347/fd7f6f51d59d/medicina-60-01713-g001.jpg

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