<i>Litchi chinensis</i> seed prevents obesity and modulates the gut microbiota and mycobiota compositions in high-fat diet-induced obese zebrafish

Xiang, Jun; Chi, Yan-Yu; Han, Jin-Xin; Kong, Ping; Liang, Zehua; Wang, Deli; Xiang, Hongyu; Xie, Qiuhong

doi:10.1039/d1fo03991a

Cited by 17 publications

(10 citation statements)

References 69 publications

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“…The non-digestible carbohydrates or some amino acids are converted into short chain FAs (SCFAs), which have multiple physiological effects on host health including lipid homeostasis ( 23 , 60 ). It is shown that Ruminococcaceae, Lachnospiraceae , and Micrococcaceae are positively correlated with obesity ( 63 ). Although fenofibrate treatment decreased the abundance of Micrococcaceae , it significantly increased the relative abundance of Ruminococcaceae and Lachnospiraceae at the family level.…”

Section: Discussionmentioning

confidence: 99%

Fenofibrate enhances lipid deposition via modulating PPARγ, SREBP-1c, and gut microbiota in ob/ob mice fed a high-fat diet

et al. 2022

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Obesity is characterized by lipid accumulation in distinct organs. Presently, fenofibrate is a commonly used triglyceride-lowering drug. This study is designed to investigate whether long-term fenofibrate intervention can attenuate lipid accumulation in ob/ob mouse, a typical model of obesity. Our data demonstrated that fenofibrate intervention significantly decreased plasma triglyceride level by 21.0%, increased liver index and hepatic triglyceride content by 31.7 and 52.1%, respectively, and elevated adipose index by 44.6% compared to the vehicle group. As a PPARα agonist, fenofibrate intervention significantly increased the expression of PPARα protein in the liver by 46.3% and enhanced the expression of LDLR protein by 3.7-fold. However, fenofibrate dramatically increased the expression of PPARγ and SREBP-1c proteins by ~2.1- and 0.9-fold in the liver, respectively. Fenofibrate showed no effects on the expression of genes-related to fatty acid β-oxidation. Of note, it significantly increased the gene expression of FAS and SCD-1. Furthermore, fenofibrate modulated the gut microbiota. Collectively, long-term fenofibrate induces lipid accumulation in liver and adipose tissues in ob/ob mice by enhancing the expression of adipogenesis-related proteins and gut microbiota. These data suggest that fenofibrate may have limited effects on attenuating lipid deposition in obese patients.

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Section: Discussionmentioning

confidence: 99%

Fenofibrate enhances lipid deposition via modulating PPARγ, SREBP-1c, and gut microbiota in ob/ob mice fed a high-fat diet

et al. 2022

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“…Additionally, a supplement of litchi pulp phenolics led to an increased abundance of the beneficial bacteria (e.g., Akkermansia , Lactobacillus , Coprococcus and Bacteroides uniformis ) and a lower abundance of harmful bacteria ( Enterococcus and Aggregatibacter ) in dextran sulfate sodium-induced colitis [ 37 ]. Moreover, a recent report indicated that litchi seed extract effectively improved obesity, insulin resistance, glucose metabolism and the intestinal barrier in animal models using a high-fat diet [ 12 ]. Litchi seed extract could also alter the gut microbiota composition through an increased proportion of SCFA-producing bacteria, such as Cetobacterium , Trichococcus , Aeromonas and Staphylococcus [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, a recent report indicated that litchi seed extract effectively improved obesity, insulin resistance, glucose metabolism and the intestinal barrier in animal models using a high-fat diet [ 12 ]. Litchi seed extract could also alter the gut microbiota composition through an increased proportion of SCFA-producing bacteria, such as Cetobacterium , Trichococcus , Aeromonas and Staphylococcus [ 12 ]. Despite the observations in pre-clinical studies, the putative effects of litchi-derived products in modulating gut microbiota might not directly translate into humans.…”

Section: Discussionmentioning

confidence: 99%

“…It was previously shown in alcohol-fed mice that the phenolic extract from litchi pulp could protect against liver injury by alleviating gut microbiota dysbiosis and intestinal barrier dysfunction [ 11 ]. Recent data also revealed that litchi seed extract could prevent obesity and altered the gut microbiota compositions in an animal model [ 12 ]. These preclinical results provide promising evidence supporting the use of litchi components as dietary supplements for the treatment of obesity and NAFLD by modulating gut dysbiosis.…”

Section: Introductionmentioning

confidence: 99%

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Litchi-Derived Polyphenol Alleviates Liver Steatosis and Gut Dysbiosis in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized Double-Blinded, Placebo-Controlled Study

et al. 2022

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Preclinical data suggest the role of litchi extract in alleviating non-alcoholic fatty liver disease (NAFLD) by modulating gut microbiota. We aimed at investigating whether oligonol, a litchi-derived polyphenol, could improve liver steatosis and gut dysbiosis in patients with NAFLD. Adults with grade ≥2 steatosis, defined by an MRI proton density fat fraction (MRI-PDFF) of ≥11%, were randomly assigned to receive either oligonol or placebo for 24 weeks. The alteration in the MRI-PDFF and gut microbiota composition assessed by 16S ribosomal RNA sequencing were examined. There were 38 patients enrolled (n = 19 in each group). A significant reduction in the MRI-PDFF between week 0 and week 24 was observed in the oligonol group, while there was a non-significant decrease in the placebo group. A significant improvement in alpha-diversity was demonstrated in both of the groups. The oligonol-induced microbiota changes were characterized by reduced abundance of pathogenic bacteria, including Dorea, Romboutsia, Erysipelotrichaceae UCG-003 and Agathobacter, as well as increased abundance of short-chain fatty acids (SCFAs)-producing bacteria, such as Akkermansia, Lachnospira, Dialister and Faecalibacterium. In summary, this study is the first to provide evidence that supports that oligonol improves steatosis through the modulation of gut bacterial composition. Our results also support the beneficial and complementary role of oligonol in treating NAFLD.

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“…Several studies have found zebrafish serve as a useful animal model of human HFD-induced obesity for research into the alterations of gut microbiota community and inflammation driven by HFD due to its similarity of organs to humans, the availability of a complete genome sequence, and its highly conserved physiological pathways ( 2 , 38 – 43 ). Although zebrafish is dominated by Proteobacteria, mice and human are dominated by Firmicutes and Bacteroidetes, the response to microbiota colonization are similar ( 44 ).…”

Section: Introductionmentioning

confidence: 99%

Pediococcus pentosaceus PR-1 modulates high-fat-died-induced alterations in gut microbiota, inflammation, and lipid metabolism in zebrafish

et al. 2023

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IntroductionObesity is a health issue worldwide. This study aimed to evaluate the beneficial effects of Pediococcus pentococcus PR-1 on the modulating of gut microbiota, inflammation and lipid metabolism in high-fat-diet (HFD)-fed zebrafish.MethodsAdult zebrafish were fed a commercial (C), high fat (H, 25% fat), probiotic (P, 106 CFU/g), or high fat with probiotic (HP) diets twice daily for 5 weeks. Gut microbiota were analysed using 16S rRNA gene sequencing. Gene expressions of intestinal cytokine, intestinal TJ protein, and liver lipid metabolism were analysed by quantitative real-time polymerase chain reaction. Biochemical and histological analysis were also performed.Results and discussionP. pentosaceus PR-1 reduced body weight and BMI, indicating its anti-obesity effect. The 16S rRNA sequencing results showed HFD induced a distinct gut microbiota structure from C group, which was restored by probiotic. P. pentosaceus PR-1 improved gut health by decreasing the abundance of Ralstonia and Aeromonas which were increased induced by HFD. Moreover, probiotic restored abundance of Fusobacteria, Cetobacterium and Plesiomonas, which were decreased in HFD-fed zebrafish. The results of quantitative real-time polymerase chain reaction showed probiotic suppressed HFD-induced inflammation by decreasing the expressions of IL-1b and IL-6. Levels of hepatic TNF-α, IL-1ß, and IL-6 were reduced by probiotic in HFD-fed zebrafish. Probiotic also ameliorated gut barrier function by increasing the expressions of occludin, Claudin-1, and ZO-1. Probiotic exerted anti-adipogenic activity through regulating the expressions of SREBP1, FAS and LEPTIN. Levels of hepatic triglyceride, total cholesterol, low density lipoprotein were also reduced by probiotic. Histological analysis showed probiotic alleviated liver steatosis and injury induced by HFD. P. pentosaceus PR-1 might be useful as a dietary health supplement, especially for reducing obesity.

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Litchi chinensis seed prevents obesity and modulates the gut microbiota and mycobiota compositions in high-fat diet-induced obese zebrafish

Abstract: Obesity continues to be a global public health challenge. Litchi chinensis seed is rich in bioactive ingredients with pharmacological effects, such as hypoglycemic activity and anti-oxidation. This study aimed to...

Cited by 17 publications

References 69 publications

Fenofibrate enhances lipid deposition via modulating PPARγ, SREBP-1c, and gut microbiota in ob/ob mice fed a high-fat diet

Fenofibrate enhances lipid deposition via modulating PPARγ, SREBP-1c, and gut microbiota in ob/ob mice fed a high-fat diet

Litchi-Derived Polyphenol Alleviates Liver Steatosis and Gut Dysbiosis in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized Double-Blinded, Placebo-Controlled Study

Pediococcus pentosaceus PR-1 modulates high-fat-died-induced alterations in gut microbiota, inflammation, and lipid metabolism in zebrafish

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