scholarly journals Modulation of Gut Microbiota by Lonicera caerulea L. Berry Polyphenols in a Mouse Model of Fatty Liver Induced by High Fat Diet

Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3213 ◽  
Author(s):  
Shusong Wu ◽  
Ruizhi Hu ◽  
Hironobu Nakano ◽  
Keyu Chen ◽  
Ming Liu ◽  
...  

Polyphenols from the Lonicera caerulea L. berry have shown protective effects on experimental non-alcoholic fatty liver disease (NAFLD) in our previous studies. As endotoxins from gut bacteria are considered to be the major trigger of inflammation in NAFLD, this study aims to clarify the regulatory effects of L. caerulea L. berry polyphenols (LCBP) on gut microbiota in a high fat diet (HFD)-induced mouse model. C57BL/6N mice were fed with a normal diet, HFD, or HFD containing 0.5–1% of LCBP for 45 days. The results revealed that supplementation with LCBP decreased significantly the levels of IL-2, IL-6, MCP-1, and TNF-α in serum, as well as endotoxin levels in both serum and liver in HFD-fed mice. Fecal microbiota characterization by high throughput 16S rRNA gene sequencing revealed that a HFD increased the Firmicutes/Bacteroidetes ratio, and LCBP reduced this ratio by increasing the relative abundance of Bacteroides, Parabacteroides, and another two undefined bacterial genera belonging to the order of Bacteroidales and family of Rikenellaceae, and also by decreasing the relative abundance of six bacterial genera belonging to the phylum Firmicutes, including Staphylococcus, Lactobacillus, Ruminococcus, and Oscillospira. These data demonstrated that LCBP potentially attenuated inflammation in NAFLD through modulation of gut microbiota, especially the ratio of Firmicutes to Bacteroidetes.

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 482
Author(s):  
Jae-Kwon Jo ◽  
Seung-Ho Seo ◽  
Seong-Eun Park ◽  
Hyun-Woo Kim ◽  
Eun-Ju Kim ◽  
...  

Obesity can be caused by microbes producing metabolites; it is thus important to determine the correlation between gut microbes and metabolites. This study aimed to identify gut microbiota-metabolomic signatures that change with a high-fat diet and understand the underlying mechanisms. To investigate the profiles of the gut microbiota and metabolites that changed after a 60% fat diet for 8 weeks, 16S rRNA gene amplicon sequencing and gas chromatography-mass spectrometry (GC-MS)-based metabolomic analyses were performed. Mice belonging to the HFD group showed a significant decrease in the relative abundance of Bacteroidetes but an increase in the relative abundance of Firmicutes compared to the control group. The relative abundance of Firmicutes, such as Lactococcus, Blautia, Lachnoclostridium, Oscillibacter, Ruminiclostridium, Harryflintia, Lactobacillus, Oscillospira, and Erysipelatoclostridium, was significantly higher in the HFD group than in the control group. The increased relative abundance of Firmicutes in the HFD group was positively correlated with fecal ribose, hypoxanthine, fructose, glycolic acid, ornithine, serum inositol, tyrosine, and glycine. Metabolic pathways affected by a high fat diet on serum were involved in aminoacyl-tRNA biosynthesis, glycine, serine and threonine metabolism, cysteine and methionine metabolism, glyoxylate and dicarboxylate metabolism, and phenylalanine, tyrosine, and trypto-phan biosynthesis. This study provides insight into the dysbiosis of gut microbiota and metabolites altered by HFD and may help to understand the mechanisms underlying obesity mediated by gut microbiota.


2020 ◽  
Vol 11 (4) ◽  
pp. 2953-2968 ◽  
Author(s):  
Xiaobing Yang ◽  
Wenjing Mo ◽  
Chuanjin Zheng ◽  
Wenzhi Li ◽  
Jian Tang ◽  
...  

Non-alcoholic fatty liver disease is associated with gut microbiota, oxidative stress, and inflammation.


2017 ◽  
Vol 8 (10) ◽  
pp. 3542-3552 ◽  
Author(s):  
F. J. García-Alonso ◽  
R. González-Barrio ◽  
G. Martín-Pozuelo ◽  
N. Hidalgo ◽  
I. Navarro-González ◽  
...  

Tomato juice intake partially ameliorated high-fat diet-induced disturbances of gut microbiota, particularly by increasingLactobacillusabundance and diminishing the acetate to propionate ratio.


2021 ◽  
Vol 10 (3) ◽  
pp. 3219-3234
Author(s):  
Yiqun Wang ◽  
Shengxia Lv ◽  
Tianbai Shen ◽  
Minchao Ye ◽  
Dehe Wang ◽  
...  

2021 ◽  
Vol 108 (Supplement_4) ◽  
Author(s):  
L Orci ◽  
S Lacotte ◽  
Q Gex ◽  
V Lazarevic ◽  
J Schrenzel ◽  
...  

Abstract Objective There is growing evidence supporting that the gut microbiota is a major driver of human health and disease. While gut microbiota transfer (GMT) is commonly used as an approach to restore "eubiosis", there is a surprising lack of data on whether the transferred microbiota efficiently and durably repopulate the gut of the transplanted subject. Moreover, little is known on the effects of GMT on non-alcoholic fatty liver disease (NAFLD). Methods Chronic dysbiosis and NAFLD-like liver injury were induced by feeding C57Bl/6j mice for 16 weeks with a high-fat diet. For GMT, dysbiotic mice underwent preliminary gut cleansing, followed by oral gavage with a suspension of fresh fecal matter procured from a pool of lean mice (1 dose, or 10 doses). We next characterized microbiota composition and we measured the relative abundance of specific pathobionts in recipient mice, using high-throughput shotgun analysis in a dynamic manner, over time. All experiments took place in a specific germ-free environment. Results After 4 months on a high-fat diet, mice displayed fatty liver infiltration with moderate parenchymal inflammatory changes. Dysbiosis was evidenced by a reduced bacterial diversity, as well as a dramatically increased abundance of Firmicutes, and lower Verrucomicrobia and Actinobacteria. Gut microbiota transfer was associated with a transitory reduction in NAFLD-induced hepatocellular injury. While dysbiotic mice displayed a shift in their microbiota composition towards that of lean donors after GMT, this effect rapidly faded after one week, and mice recovered their initial, dysbiotic microbiota. Conclusion The current study indicates that, when used in mice with chronically established dysbiosis, GMT is merely associated with transitory changes in gut microbiota composition, as well as significant but moderate reduction in hepatocellular injury.


Background and Aims: Non-alcoholic fatty liver disease (NAFLD) is associated with such symptoms as steatosis, fibrosis, and liver cirrhosis. Kelussia has attracted assiduous attention due to its protective effects on the liver. The PNPLA3 gene is mainly expressed in the liver and plays a major role in the degradation rate of hepatic triglycerides. Therefore, the present study aimed to assess the effect of Kelussia extract on PNPLA3 gene expression in rats with fatty liver and healthy rats. Materials and Methods: This experimental study was conducted on 24 male Wistar rats in the control group (no treatment), obese group (which received a high-fat diet), treatment group 1 (which received a high-fat diet with Kelussia extract 400 mg/kg) and treatment group 2 (a high-fat diet with Kelussia extract 800 mg/kg) for six weeks. Blood samples were taken from rats and the factors of (LDL, HDL, Cholesterol, Triglyceride, and fasting sugar) were measured. After sampling the rat liver, the effect of Kelussia on PNPLA3 gene expression was investigated using the Real-time reverse transcription-polymerase chain reaction (RT-PCR) technique and analyzed in SPSS software (version 22). Results: Based on the results, Kelussia extract at a dose of 800 mg/kg resulted in a more dramatic decrease in PNPLA3 gene expression in rats with fatty liver, compared to a dose of 400 mg /kg, and this reduction was statistically significant, compared to the fatty liver group (P<0.05). The results of biochemical tests confirmed liver improvement in the rats treated with Kelussia extract at a dose of 800 mg/kg. Conclusion: It can be said that Kelussia had a beneficial effect on the reduction of blood lipids; moreover, it reduces the accumulation of triglycerides in the liver and improves the tissue structure of the liver by reducing the expression of PNPLA3 gene; therefore, with more studies, it can be considered a supplement to reduce blood lipids.


2020 ◽  
Vol 32 (5) ◽  
pp. 2603-2609
Author(s):  
Yuzhen Wang ◽  
Jimin Zheng ◽  
Hongtao Hou ◽  
Jian Zhang ◽  
Shuangfei Qi ◽  
...  

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