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补充益生菌通过调节肉鸡肝脏脂肪生成和增加肠道微生物群多样性来缓解皮质酮诱导的脂肪肝疾病。

Probiotic Supplementation Alleviates Corticosterone-Induced Fatty Liver Disease by Regulating Hepatic Lipogenesis and Increasing Gut Microbiota Diversity in Broilers.

作者信息

Feng Yuyan, Mei Wenqing, Chen Qu, Chen Xiaojing, Ni Yingdong, Lei Mingming, Liu Jie

机构信息

Institute of Animal Husbandry, Jiangsu Academy of Agricultural Sciences, Nanjing 210094, China.

Key Laboratory of Animal Physiologic and Biochemistry, College of Veterinary Medicine, Ministry of Agriculture and Rural Affairs, Nanjing Agricultural University, Nanjing 210094, China.

出版信息

Microorganisms. 2025 Jan 17;13(1):200. doi: 10.3390/microorganisms13010200.

Abstract

Emerging evidence indicates a close relationship between gut microbiota and fatty liver disease. It has been suggested that gut microbiota modulation with probiotics ameliorates fatty liver disease in rodents and humans, yet it remains unclear whether the same results will also be obtained in poultry. The aim of this study was to investigate whether a mixture of probiotics supplemented after hatching can prevent CORT-induced fatty liver disease in broilers, and to determine how such effects, if any, are associated with hepatic de novo lipogenesis and gut microbiota composition. Ninety-six one-day-old green-legged chickens were divided into a control group (CON) and probiotic group (PB). At 28 days of age, fatty liver was induced in 16 broilers that were randomly selected from the CON or PB group. At the end of the experiment, broilers from four groups, (i) the control group (CON), (ii) corticosterone group (CORT), (iii) probiotic group (PB), and (iv) PB plus CORT group (CORT&PB), were slaughtered for sampling and analysis. The results showed that probiotic administration significantly prevented CORT-induced body weight loss ( < 0.05) but did not alleviate the weight loss of immune organs caused by CORT. Compared to CON, the broilers in the CORT group exhibited a significant increase in triglyceride (TG) levels in plasma and liver ( < 0.01), as well as severe hepatocytic steatosis and hepatocellular ballooning, which was accompanied by the upregulation of hepatic lipogenesis gene expression. However, probiotic supplementation markedly decreased the intrahepatic lipid accumulation and steatosis histological score, which was associated with the downregulation of sterol regulatory element-binding protein-1 () and acetyl-CoA carboxylase () mRNA ( < 0.05) and the expression of its protein ( = 0.06). The cecal microbiota composition was determined by 16S rRNA high-throughput sequencing. The results showed that CORT treatment induced distinct gut microbiota alterations with a decrease in microbial diversity and an increase in abundance ( < 0.05). In contrast, probiotic supplementation increased the beta diversity, the community richness, and the diversity index ( > 0.05), as well as the abundance of ( < 0.05). Our results indicate that CORT treatment induced severe fatty liver disease and altered the gut microbiota composition in broilers. However, post-hatching probiotic supplementation had a beneficial effect on alleviating fatty liver disease by regulating lipogenic gene expression and increasing gut microbiota diversity and the abundance of beneficial bacteria. We demonstrate for the first time that the supplementation of probiotics to chicks had a beneficial effect on preventing fatty liver disease through regulating lipogenic gene expression and improving the gut microbial balance. Thus, our results indicate that probiotics are a potential nutritional agent for preventing fatty liver disease in chickens.

摘要

新出现的证据表明肠道微生物群与脂肪肝疾病之间存在密切关系。有人提出,用益生菌调节肠道微生物群可改善啮齿动物和人类的脂肪肝疾病,但在家禽中是否也能得到相同的结果仍不清楚。本研究的目的是调查孵化后补充益生菌混合物是否能预防肉鸡因皮质酮(CORT)诱导的脂肪肝疾病,并确定这种影响(如果有的话)与肝脏从头脂肪生成和肠道微生物群组成之间的关系。96只1日龄的绿脚鸡被分为对照组(CON)和益生菌组(PB)。在28日龄时,从CON组或PB组中随机选择16只肉鸡诱导其发生脂肪肝。在实验结束时,对四组肉鸡进行屠宰取样和分析,这四组分别为:(i)对照组(CON)、(ii)皮质酮组(CORT)、(iii)益生菌组(PB)和(iv)PB加CORT组(CORT&PB)。结果表明,施用益生菌显著预防了CORT诱导的体重减轻(P<0.05),但并未减轻CORT引起的免疫器官体重减轻。与CON组相比,CORT组肉鸡血浆和肝脏中的甘油三酯(TG)水平显著升高(P<0.01),同时伴有严重的肝细胞脂肪变性和肝细胞气球样变,并伴随着肝脏脂肪生成基因表达的上调。然而,补充益生菌显著降低了肝内脂质积累和脂肪变性组织学评分,这与固醇调节元件结合蛋白-1(SREBP-1)和乙酰辅酶A羧化酶(ACC)mRNA的下调(P<0.05)及其蛋白表达(P = 0.06)有关。通过16S rRNA高通量测序确定盲肠微生物群组成。结果表明,CORT处理诱导了明显的肠道微生物群改变,微生物多样性降低,[某种细菌名称]丰度增加(P<0.05)。相比之下,补充益生菌增加了β多样性、群落丰富度和多样性指数(P>0.05),以及[某种有益细菌名称]的丰度(P<0.05)。我们的结果表明,CORT处理诱导了肉鸡严重的脂肪肝疾病并改变了肠道微生物群组成。然而,孵化后补充益生菌通过调节脂肪生成基因表达、增加肠道微生物群多样性和有益细菌的丰度,对减轻脂肪肝疾病具有有益作用。我们首次证明,给雏鸡补充益生菌对预防脂肪肝疾病具有有益作用,其机制是通过调节脂肪生成基因表达和改善肠道微生物平衡。因此,我们的结果表明,益生菌是预防鸡脂肪肝疾病的一种潜在营养剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd4c/11767375/a075054d66ae/microorganisms-13-00200-g001.jpg

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