Curcumin alleviates high-fat diet-induced hepatic steatosis and obesity in association with modulation of gut microbiota in mice

Li, Shuo; You, Jinming; Wang, Zirui; Liu, Yue; Wang, Bo; Du, Min; Zou, Tiande

doi:10.1016/j.foodres.2021.110270

Cited by 113 publications

(79 citation statements)

References 56 publications

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“…Based on these studies, there remains a great demand for the development of safe and effective microbiota-targeted treatments for metabolic syndrome. An increasing amount of evidence has shown that dietary flavonoids, such as camu, citrus, myricetin, and curcumin ( Anhe et al, 2019 ; Zeng et al, 2020 ; Li et al, 2021 ; Sun et al, 2021 ), are not totally absorbed by the intestinal tract and can be metabolized by the intestinal microbiota, indicating that flavonoids may dominate in the maintenance of gut health ( Gil-Cardoso et al, 2016 ). Api, one of the naturally occurring flavonoids that exists in daily fruits and vegetables, like plant-derived beverages, grapefruit, celery, parsley, and onions, has aroused research interests in recent years for health promotion benefiting from its negligible intrinsic toxicity, antioxidant, and anticancer properties ( Shao et al, 2013 ; Feng et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Apigenin Alleviates Obesity-Associated Metabolic Syndrome by Regulating the Composition of the Gut Microbiome

et al. 2022

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The gut microbiota, often viewed as a “digestive organ,” can influence the development of obesity and related metabolic disorders. Diet is significantly important in shaping the structure and modulating the function of the gut microbiota. Apigenin (Api) widely exists in fruits and vegetables as a naturally occurring flavonoid and has anti-obesogenic, anti-inflammatory, and anti-carcinogenic properties. Its low bioavailability means it has enough time to interact with the intestine thus becomes a potential substrate for the gut intestine; thus, contributing to gut health. Here, we show that Api reduces whole-body weight, low-grade inflammation, and insulin resistance in high-fat diet (HFD)-induced obese mice. Our results reflect that Api supplementation can substantially improve intestinal dysbiosis triggered by HFD and restores gut barrier damage by alleviating metabolic endotoxemia. Augmentation of Akkermansia and Incertae_Sedis along with reduction of Faecalibaculum and Dubosiella at the genus level potentially mediated the protective effects of Api on metabolic syndrome. Furthermore, we show that the impact of Api on the reduction of body weight and the modification of gut microbiota could be transferred from Api-administered mice to HFD-feeding mice via horizontal fecal microbiota transplantation. Taken together, our data highlight the prebiotic role of Api and show its contribution to the restraint of gut dysbiosis and metabolic deterioration associated with obesity in mice.

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Section: Discussionmentioning

confidence: 99%

Apigenin Alleviates Obesity-Associated Metabolic Syndrome by Regulating the Composition of the Gut Microbiome

et al. 2022

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“…In the 16s rDNA sequencing analysis, an increase of Firmicutes/Bacteroidetes (F/B) ratio was found in the HFD group, which was also observed in ovariectomized mice with bone loss ( Wen et al., 2020 ; Xie et al., 2020 ) and people with primary osteoporosis ( Wang et al., 2017 ). Previous studies addressing obesity or nonalcoholic fatty liver disease have also demonstrated that HFD can induce an increase in F/B ratio ( Li et al., 2021 ), which is closely related to intestinal immune inflammation ( Zhao et al., 2021 ). In addition, HFD also led to a decrease in the abundance of SCFA-producing bacteria, such as Bacteroides , which exerts a bone protection effect via both promoting osteoblast differentiation ( Chen et al., 2007 ) and inhibiting osteoclast differentiation ( Lucas et al., 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota and Serum Metabolic Signatures of High-Fat-Induced Bone Loss in Mice

Tang

Jiao

et al. 2021

Front. Cell. Infect. Microbiol.

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BackgroundAccumulating evidence indicates that high-fat diet (HFD) is a controllable risk factor for osteoporosis, but the underlying mechanism remains to be elucidated. As a primary biological barrier for nutrient entry into the human body, the composition and function of gut microbiota (GM) can be altered rapidly by HFD, which may trigger abnormal bone metabolism. In the current study, we analyzed the signatures of GM and serum metabolomics in HFD-induced bone loss and explored the potential correlations of GM and serum metabolites on HFD-related bone loss.MethodsWe conducted a mouse model with HFD-induced bone loss through a 12-week diet intervention. Micro-CT, Osmium-μCT, and histological analyses were used to observe bone microstructure and bone marrow adipose tissue. Quantitative Real-Time PCR was applied to analyze gene expression related to osteogenesis, adipogenesis, and osteoclastogenesis. Enzyme-linked immunosorbent assay was used to measure the biochemical markers of bone turnover. 16s rDNA sequencing was employed to analyze the abundance of GM, and UHPLC-MS/MS was used to identify serum metabolites. Correlation analysis was performed to explore the relationships among bone phenotypes, GM, and the metabolome.ResultsHFD induced bone loss accompanied by bone marrow adipose tissue expansion and bone formation inhibition. In the HFD group, the relative abundance of Firmicutes was increased significantly, while Bacteroidetes, Actinobacteria, Epsilonbacteraeota, and Patescibacteria were decreased compared with the ND group. Association analysis showed that thirty-two bacterial genera were significantly related to bone volume per tissue volume (BV/TV). One hundred and forty-five serum metabolites were identified as differential metabolites associated with HFD intervention, which were significantly enriched in five pathways, such as purine metabolism, regulation of lipolysis in adipocyte and cGMP-PKG signaling pathway. Sixty-four diffiential metabolites were matched to the MS2 spectra; and ten of them were positively correlated with BV/TV and five were negatively correlated with BV/TV.ConclusionsThese findings indicated that the alternations of GM and serum metabolites were related to HFD-induced bone loss, which might provide new insights into explain the occurrence and development of HFD-related osteoporosis. The regulatory effects of GM and metabolites associated with HFD on bone homeostasis required further exploration.

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“…In the present study, we observed a remarkable increase in the abundance of Lachnospiraceae_NK4A136_group in the HFC group, suggesting that CPP supplementation protects the intestinal mucosa and reduces the occurrence of inflammation. Li et al suggested that Desulfovibrio can promote lipopolysaccharide (LPS) production and thus induce intestinal inflammation [ 52 ]. Chen et al concluded that Desulfovibrio was not always associated with adverse health effects and that Desulfovibrio was negatively associated with BMI (body mass index), UA (uric acid), TG, and waist measurements, which are indicators of obesity or metabolic disorders [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

The Regulatory Effects of Citrus Peel Powder on Liver Metabolites and Gut Flora in Mice with Non-Alcoholic Fatty Liver Disease (NAFLD)

Zhang

Ruan

et al. 2021

Foods

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Gannan navel orange and Jinggang pomelo, belonging to the genus Citrus, are good sources of phenolic compounds, which are mainly concentrated in the peel. These phenolic compounds are considered promising in the prevention and treatment of non-alcoholic fatty liver disease (NAFLD). In order to maximize nutrients retention and bioactivity in the peel, pomelo peel and orange peel were processed using freeze-drying technology and mixed in the ratio (pomelo peel powder 50% and orange peel powder 50%) to make citrus peel powder (CPP). The purpose of this study was to explore new strategies and mechanisms associated with the consumption of CPP to alleviate nonalcoholic fatty liver injury, lipid metabolism disorders, and gut microbiota dysbiosis in obese mice induced by high-fat diet (HFD). The results showed that after 12 weeks of CPP administration, CPP supplementation had a strong inhibitory effect on HFD-induced weight gain, hepatic fat accumulation, dyslipidemia, and the release of pro-inflammatory cytokines. In particular, CPP modulates the composition of the intestinal flora, such as increasing the relative abundance of phylum Firmicutes, genus Faecalibaculum, genus Lactobacillus, genus Dubosiella, and genus Lachnospiraceae_NK4A136_ group and decreasing the relative abundance of phylum Bacteroidota, genus Helicobacter, and genus Bacteroides. These results suggest that CPP has a preventive effect on NAFLD, which can be related to the regulation of intestinal flora.

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Curcumin alleviates high-fat diet-induced hepatic steatosis and obesity in association with modulation of gut microbiota in mice

Cited by 113 publications

References 56 publications

Apigenin Alleviates Obesity-Associated Metabolic Syndrome by Regulating the Composition of the Gut Microbiome

Apigenin Alleviates Obesity-Associated Metabolic Syndrome by Regulating the Composition of the Gut Microbiome

Gut Microbiota and Serum Metabolic Signatures of High-Fat-Induced Bone Loss in Mice

The Regulatory Effects of Citrus Peel Powder on Liver Metabolites and Gut Flora in Mice with Non-Alcoholic Fatty Liver Disease (NAFLD)

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