Journal of Functional Foods
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2020
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IF 3.701
Fengfeng Mei,Zhouwei Duan,Muxue Chen,Jinfeng Lu,Meihui Zhao,Laihao Li,Xuanri Shen,Guanghua Xia,Shengjun Chen
In this study, a total of 24 male Sprague Dawley rats were randomly divided into 3 group (Collagen peptide of Salmon salar skin group, Ss- SCP ; Collagen peptide of Tilapia nilotica skin group, Tn -SCP and Model control group, MC) to investigate the impact of a high-collagen peptide diet on the gut microbiota and host health. After 16 days intervention, the body weights of the Ss -SCP and Tn -SCP intervention groups were significantly increased and the liver index was also remarkably higher than that of the MC group. The acetic acid and propionic acid levels in feces were both significantly increased in the diet high-collagen peptide groups and valerate acid level was lower than that in the MC group. With the intervention of a high-dose collagen peptide diet, the gut microbiota of the groups was shifted with increased abundance of Lactobacillus , Unidentified-Prevotellaceae , Allobaculum, and Parasutterella , whereas the Tn -SCP administration have caused low abundance of Anaerostipes, Blautia, and Fusicatenibacter . The relative abundance of Allobaculum as well as Parasutterella was positively correlated with propionic acid and acetic acid levels, respectively. In addition, Allobaculum abundance was negatively correlated with valerate acid level. The serum valerate acid content was potentially harmful to rat health and significantly increased in the groups intervened with collagen peptide. All together, these results showed that administration of diet high-collagen peptide shifts the gut microbiota in rats and induced a disturbance in short-chain fatty acid metabolism which is potentially harmful to health.
研究领域:
营养学
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微生物学
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胃肠病学
✓ 已验证
产品关联
DOI
高影响因子
Frontiers in Microbiology
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2024
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IF 4
Xinwen Dong,Yaguang Su,Zheng Luo,Cuiying Li,Jie Gao,Xiaofeng Han,Sanqiao Yao,Weidong Wu,Linqiang Tian,Yichun Bai,Guizhi Wang,Wenjie Ren
Background: Dysbiosis of gut microbiota (GM) is intricately linked with cognitive impairment and the incidence of traumatic brain injury (TBI) in both animal models and human subjects. However, there is limited understanding of the impact and mechanisms of fecal microbiota transplantation (FMT) on brain and gut barrier function in the treatment of TBI induced by gas explosion (GE).Methods: We have employed FMT technology to establish models of gut microbiota dysbiosis in male rats, and subsequently conducted non-targeted metabolomics and microbiota diversity analysis to explore the bacteria with potential functional roles.Results: Hematoxylin–eosin and transmission electron microscopy revealed that GE induced significant pathological damage and inflammation responses, as well as varying degrees of mitochondrial impairment in neuronal cells in the brains of rats, which was associated with cognitive decline. Furthermore, GE markedly elevated the levels of regulatory T cell (Tregs)-related factors interleukin-10, programmed death 1, and fork head box protein P3 in the brains of rats. Similar changes in these indicators were also observed in the colon; however, these alterations were reversed upon transfer of normal flora into the GE-exposed rats. Combined microbiome and metabolome analysis indicated up-regulation of Clostridium_T and Allobaculum, along with activation of fatty acid biosynthesis after FMT. Correlation network analysis indirectly suggested a causal relationship between FMT and alleviation of GE-induced TBI. FMT improved intestinal structure and up-regulated expression of tight junction proteins Claudin-1, Occludin, and ZO-1, potentially contributing to its protective effects on both brain and gut.Conclusion: Transplantation of gut microbiota from healthy rats significantly enhanced cognitive function in male rats with traumatic brain injury caused by a gas explosion, through the modulation of gut microbiome composition and the improvement of both gut and brain barrier integrity via the gut-brain axis. These findings may offer a scientific foundation for potential clinical interventions targeting gas explosion-induced TBI using FMT.
研究领域:
神经科学
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微生物学
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药理学
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代谢组学
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病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF FOOD SCIENCE
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2024
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IF 3.2
Junwei Zhang,Yu Zhong,Danfeng Wang,Jiangxiong Zhu,Yun Deng,Yuncheng Li,Cong Liu,Ji-Li-Te Wang,Minyan Zhang
Fermented foods have shown promise in preventing or treating ulcerative colitis (UC) via regulating intestinal flora and correcting metabolic disorders. However, the prevention effect of fermented Wallace melon juice (FMJ) on UC is unclear. In this study, the effects of FMJ on dextran sodium sulfate (DSS)-induced UC were investigated via 16S rRNA sequencing and non-targeted metabolomics. The results showed that FMJ was effective in alleviating the symptoms of UC, reducing histological damage and oxidative stress, decreasing the levels of pro-inflammatory cytokines. After FMJ treatment, the level of propionic acid, butyric acid, and valeric acid increased by 14.1%, 44.4%, and 52.4% compared to DSS-induced UC mice. Meanwhile, the levels of harmful bacteria such as Oscillospira , Bacteroidetes , and Erysipelotrichaceae and Clostridium decreased, while the levels of beneficial bacteria such as Akkermansia , Lactobacillus , and Bifidobacterium increased. Fecal metabolomics analysis identified 31 differential metabolites, which could regulate metabolic disorders in UC mice by controlling the primary bile acid biosynthesis, purine metabolism, and pantothenate and CoA biosynthesis pathway. Additionally, the abundances of butyric acid, bile acids, and pantothenic acid were positively correlated with Allobaculum, Bifidobacterium , and other beneficial bacteria ( R 2 > 0.80, p < 0.01). The results indicated that FMJ played a role in regulating the structure of intestinal flora, which in turn helped in repairing metabolic disorders and alleviated colitis inflammation.
研究领域:
胃肠病学
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微生物学
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代谢组学
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营养科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
SCIENCE OF THE TOTAL ENVIRONMENT
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2021
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IF 7.963
Cuiyuan Jin,You Weng,Yi Zhang,Zhiwei Bao,Guiling Yang,Zhengwei Fu,Yuanxiang Jin
Propamocarb is a systemic carbamate fungicide used to fight diseases. The effect of propamocarb on the formation of atherosclerosis was evaluated in wild-type (WT) and ApoE knockout (ApoE −/− ) mice. C57BL/6 J WT mice were fed control diet or high-fat diet (HFD) with 20 mg/L propamocarb in drinking water for 24 weeks. Propamocarb significantly increased the serum levels of triglyceride, cholesterol and low-density lipoprotein cholesterol while decreasing high-density lipoprotein cholesterol. Simultaneously, propamocarb facilitated lipid accumulation in the liver and increased the expression of cholesterol synthesis and transport genes in the liver and ileum. Lipid accumulation was observed in the aortic roots of the propamocarb-treated mice fed HFD, and similar results were also observed with whole aorta staining. In addition, propamocarb exposure significantly increased the mRNA levels of IL-1β , TNF-α , ICAM-1 , and VCAM-1 in the aorta and the serum IL-1β, IL-6, and TNF-α levels in HFD groups treated with propamocarb. In ApoE −/− mice, the results were consistent with those obtained in WT mice after exposure to 20 mg/L propamocarb for 10 weeks. Meanwhile, propamocarb significantly increased the levels of CD36, NF-κB, VCAM-1 and ICAM-1 proteins in the aortas of ApoE −/− mice. Propamocarb further disrupted cholesterol metabolism and enhanced atherosclerosis and inflammatory responses much more substantially, indicating that propamocarb has the potential to accelerate the formation of atherosclerosis. An analysis of gut microbiota revealed that propamocarb altered the composition of gut microbiota in both WT and ApoE −/− mice. Interestingly, propamocarb increased the abundance of Peptostreptococcaceae, Ruminococcaceae, and Clostridiales_VadinBB60_group , which are related to atherosclerosis at the family level. The abundance of Paeniclostridium, Allobaculum, and Clostridioides , which are closely related to atherosclerosis, was also increased by propamocarb exposure. Our findings indicate that propamocarb exposure may promote atherosclerosis by disrupting lipid metabolism, increasing the inflammatory response, and altering the structure of gut microbiota.
研究领域:
药理学
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心血管疾病
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免疫学
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微生物学
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代谢
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CARBOHYDRATE POLYMERS
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2022
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IF 10.723
Wangting Zhou,Tingting Yang,Weiqi Xu,Yujie Huang,Linwu Ran,Yamei Yan,Jia Mi,Lu Lu,Yi Sun,Xiaoxiong Zeng,Youlong Cao
The antidiabetic effect and potential mechanisms of the polysaccharides from the fruits of Lycium barbarum L. (LBPs) by the mouse model of high-fat diet/streptozotocin-induced diabetes were investigated. Six-week oral administration of LBPs (200 mg/kg/day) resulted in improvement in the levels of fasting blood glucose (13.51% decrease) and glycated hemoglobin and β-cell function in diabetic mice, and simultaneously induced a 3.3-fold increment in one taxon belonging to genus Allobaculum in gut bacterial community. The experiments of fecal microbiota transplantation and antibiotics treatment confirmed that the LBPs-mediated gut microbiota participated in the glycemic control of the diabetes management. Moreover, LBPs intervention guarded the intestinal barrier function via upregulating the expression of zonula occludens 1 both in vivo (analyzing the gut permeability in diabetic mice) and in vitro (using intestinal-like Caco-2/RAW264.7 cells co-culture inflammation model). Collectively, our study showed that LBPs could confer anti-diabetic effect through modifying gut microbiota and intestinal barrier.
研究领域:
药理学
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微生物学
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糖尿病研究
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营养科学
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胃肠病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）