PLoS One:缘何瘦子也会得NASH-HCC?反式脂肪、胆固醇和果糖含量高的不健康饮食或是关键!

2022-08-26 MedSci原创 MedSci原创

PLoS One:肥胖和非肥胖小鼠不健康饮食诱导的肝细胞癌的差异进展

在全球范围内,非酒精性脂肪性肝病(NAFLD)的患病率为24%非酒精性脂肪性肝病(NAFLD)在西方国家的肝病中排名第一,预计到2030年将成为美国肝移植的主要原因。

NAFLD的一些危险因素包括肥胖,糖尿病和遗传易感性,然而,它也可以在没有代谢综合征的瘦人中发展。在美国,瘦人NAFLD的患病率为7%,在某些亚洲国家高达25-30%NAFLD从肝脏脂肪过量积累(NAFL)开始,发展为非酒精性脂肪性肝炎(NASH),肝硬化和肝细胞癌(HCC)。瘦 NASH-HCC 的发病机制及其与肥胖 NASH-HCC 的不同之处尚不清楚因此很难识别瘦NAFLD,并导致诊断延迟和预后不良。

因此,本研究分别使用胆碱缺乏/高反式脂肪/果糖/胆固醇饮食和胆碱补充/高反式脂肪/果糖/胆固醇饮食生成瘦肉和肥胖NASH-HCC的小鼠模型,以比较瘦小鼠与肥胖小鼠中NASH-HCC的进展。通过研究这些小鼠血浆中的脂肪酸代谢,在生物体,组织学和分子水平上进行比较。

结果表明,与瘦小鼠相比,肥胖小鼠表现出更明显的葡萄糖不耐受和胰岛素抵抗,更高水平的血浆胆固醇和甘油三酯,以及更高的NASH外显率。

尽管肥胖小鼠的代谢特征异常,但雄性肥胖小鼠和瘦小鼠发展出具有相似外显率的HCC(分别为53.3%53.8%),尽管瘦小鼠表现出更快的肿瘤进展,如较大的肿瘤大小和较低的无HCC生存率所证明的那样。没有一只雌性瘦鼠发展为HCC,而50%的雌性肥胖小鼠发展为HCC。两组小鼠都显示出血浆多不饱和脂肪酸(PUFAs)的减少。然而,与瘦小鼠相比,肥胖小鼠的水平高于终点。

在肥胖和正常体重的情况下,反式脂肪,胆固醇和果糖含量高的不健康饮食都会导致肝癌的发生。与肥胖相比,在正常体重的背景下,男性的肿瘤进展更快,女性的肿瘤进展较慢,这表明肥胖对性别的致癌作用不同。生成的小鼠模型是研究瘦和肥胖NASH-HCC以及在这两种情况下更好地了解肝癌发生机制的重要资源。

 

原文来源:

Hymel E, Vlock E, Fisher KW, Farazi PA. Differential progression of unhealthy diet-induced hepatocellular carcinoma in obese and non-obese mice. PLoS One. 2022 Aug 22;17(8):e0272623. doi: 10.1371/journal.pone.0272623. PMID: 35994501; PMCID: PMC9394802.

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    2022-08-28 jiyangfei
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    2022-08-28 kksonne
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