Gubra Amylin-NASH Diet Induced Nonalcoholic Fatty Liver Disease Associated with Histological Damage, Oxidative Stress, Immune Disorders, Gut Microbiota, and Its Metabolic Dysbiosis in Colon

IF 4.5 2区农林科学 Q1 FOOD SCIENCE & TECHNOLOGY

Molecular Nutrition & Food Research Pub Date : 2024-07-05 DOI:10.1002/mnfr.202300845

Zhimin Zhang, Xinyi Qin, Tao Yi, Yamei Li, Chengfeng Li, Min Zeng, Hongshan Luo, Xiulian Lin, Jingchen Xie, Bohou Xia, Yan Lin, Limei Lin

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Abstract

Scope

The overall changes of colon under nonalcoholic fatty liver disease (NAFLD) remain to be further elucidated.

Methods and Results

This study establishes a mouse model of NAFLD through a long-term Gubra Amylin-nonalcoholic steatohepatitis (NASH) diet (GAN diet). The results show that GAN diet significantly induces weight gain, liver steatosis, colonic oxidative stress, and lipid accumulation in blood, liver, and adipose tissue in mice. GAN feeding reduces the diversity of the gut microbiota, alters the composition and abundance of the gut microbiota, and leads to an increase in microbial metabolites such as long-chain fatty acids (LCFAs) and secondary bile acids (BAs), as well as a decrease in short-chain fatty acids (SCFAs). The RNA-seq and immunofluorescence results reveal that the GAN diet alters the expression of proteins and their coding genes involved in oxidative stress, immune response, and barrier function in colon tissue, such as lipocalin-2 (Lcn2, p < 0.05), heme oxygenase-1 (HO-1/Hmox1, p < 0.05), interferon-gamma (IFN-γ), and claudin-3/7. In addition, correlation analysis indicates a strong correlation between the changes in gut microbiota and lipid biomarkers. Additionally, the expression of immune related genes in colon tissue is related to the LCFAs produced by microbial metabolism.

Conclusion

GAN-induced NAFLD is related to microbiota and its metabolic imbalance, oxidative stress, immune disorders, and impaired barrier function in colon.

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Gubra Amylin-NASH 饮食诱发的非酒精性脂肪肝与结肠组织学损伤、氧化应激、免疫紊乱、肠道微生物群及其代谢紊乱有关。

范围：非酒精性脂肪肝（NAFLD）下结肠的整体变化仍有待进一步阐明：本研究通过长期Gubra Amylin-非酒精性脂肪性肝炎（NASH）饮食（GAN饮食）建立了非酒精性脂肪性肝炎小鼠模型。结果表明，GAN饮食能显著诱导小鼠体重增加、肝脏脂肪变性、结肠氧化应激以及血液、肝脏和脂肪组织中的脂质积累。GAN喂养降低了肠道微生物群的多样性，改变了肠道微生物群的组成和丰度，导致长链脂肪酸（LCFAs）和次级胆汁酸（BAs）等微生物代谢产物的增加，以及短链脂肪酸（SCFAs）的减少。RNA-seq和免疫荧光结果显示，GAN饮食改变了结肠组织中参与氧化应激、免疫反应和屏障功能的蛋白质及其编码基因的表达，如脂钙蛋白-2（Lcn2，p 结论）：GAN诱导的非酒精性脂肪肝与微生物群及其代谢失衡、氧化应激、免疫紊乱和结肠屏障功能受损有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Molecular Nutrition & Food Research 工程技术-食品科技

CiteScore

8.70

自引率

1.90%

发文量

250

审稿时长

1.7 months

期刊介绍： Molecular Nutrition & Food Research is a primary research journal devoted to health, safety and all aspects of molecular nutrition such as nutritional biochemistry, nutrigenomics and metabolomics aiming to link the information arising from related disciplines: Bioactivity: Nutritional and medical effects of food constituents including bioavailability and kinetics. Immunology: Understanding the interactions of food and the immune system. Microbiology: Food spoilage, food pathogens, chemical and physical approaches of fermented foods and novel microbial processes. Chemistry: Isolation and analysis of bioactive food ingredients while considering environmental aspects.