Journal of Functional Foods
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2025
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IF 4
Yan Ma,Zhengnan Jiang,Hai Xie,Jian Wang,Minni Li,Huifang Ge,Wenbin Li,Zhongwen Xie,Daxiang Li,Xueling Gao,Hongyan Wang
Fermented oxidation fresh tea (FOFT) is a unique dark tea produced by a single strain of Eurotium cristatum , and its impact on obesity has not been extensively studied. Here, we investigated the anti-obesity and metabolic benefits of FOFT using a HFD-induced obesity mouse model. The HFD-fed mice or ND-fed mice were orally administered with FOFT for 12 weeks. The results showed that FOFT invention significantly suppressed body weight gain, ameliorated liver and adipocyte morphology, and improved glucolipid metabolism and intestinal homeostasis imbalance in HFD-fed mice. Notably, FOFT administration caused no adverse effects in ND mice, indicating its safety at tested doses. Moreover, FOFT restored intestinal microbiome dysbiosis and elevated the short-chain fatty acid levels. This gut microbiome shift was associated with reduced systemic inflammation and attenuated hepatic lipid accumulation. These findings suggest that FOFT, as a novel functional food, holds great promise for resistance to obesity and its comorbidities.
研究领域:
营养学
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微生物学
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代谢生物学
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产品关联
DOI
高影响因子
Probiotics and Antimicrobial Proteins
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2024
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IF 4.4
Feng Xiaoyan,Wang Mengqi,Wen Siyue,Hu Liehai,Lan Yuzhi,Xu Hengyi
Mitigating steatosis is essential for delaying the progression of alcoholic liver disease. The effect and mechanism of Lactiplantibacillus plantarum P101 (LP.P101) on alleviating alcohol-induced hepatic lipid accumulation were investigated in our study. The mouse model was constructed by a short-term (10-day)-plus-binge ethanol feeding and gavaged with 10 8 CFU/mL of LP.P101 daily. Lipid droplet in the liver was significantly reduced by LP.101 intervention on AMPK activation. However, when AMPK was inhibited by dorsomorphin, the levels of related indicators (ALT, TG, etc.) and the expression levels of AMPK and relevant genes in the liver converged to that of the alcohol-fed group. Compared with the alcohol-fed group, LP.P101 reduced the relative abundance of Firmicutes and increased that of Bacteroidetes. Parabacteroides merdae was negatively correlated with lipid accumulation, and unclassified Negativibacillus was negatively associated with AMPK activation. Importantly, LP.P101 modified the compositions of the serum metabolites. The potential biomarker stercobilinogen was positively correlated with AMPK activation and negatively associated with lipid accumulation. This work confirmed that LP.P101 attenuated alcohol-induced hepatic lipid accumulation in mice through AMPK activation, and the alterations in gut microbiota and metabolites may play a significant role on AMPK activation.
研究领域:
肝病学
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微生物学
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代谢组学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
SCIENCE OF THE TOTAL ENVIRONMENT
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2022
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IF 10.753
Xiangjuan Wei,Daqian Yang,Boya Zhang,Xingpei Fan,Haining Du,Ruijiao Zhu,Xiaotong Sun,Meimei Zhao,Ning Gu
Di-(2-ethylhexyl) phthalate (DEHP), an endocrine-disrupting chemical (EDC) commonly used as a plasticizer, is responsible for widespread environmental pollution. Epidemiological and experimental data implicate DEHP and its metabolite mono(2-ethylhexyl) phthalate (MEHP) in the occurrence and development of metabolic syndrome. However, the specific effects and potential mechanisms of action of DEHP on glucose and lipid metabolism in adults are currently unclear. In the current study, adult male mice were continuously exposed to DEHP (0, 5, and 25 mg/kg/day) via oral administration and changes in glucose and lipid metabolism explored. Notably, exposure to DEHP led to a significant increase in plasma glucose and hepatic lipid accumulation but had no effect on insulin secretion. Western blot and real-time quantitative PCR showed that DEHP induced insulin resistance and promoted gluconeogenesis and lipid accumulation via overexpression of forkhead box protein O1 (FoxO1), in keeping with hepatic RNA sequencing data. Variations in gut microbiota aggravated these effects while inhibition of FoxO1 reversed the adverse effects of DEHP. Our findings support a key role of FoxO1 in disorders of glucose and lipid metabolism caused by DEHP.
研究领域:
内分泌学
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代谢学
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分子生物学
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环境健康
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2020
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IF 3.69
Meijing Liu,Guohui Zhang,Shuangcheng Wu,Meng Song,Jueyu Wang,Weibin Cai,Suiqing Mi,Changhui Liu
Ethnopharmacology relevance The farnesoid X receptor (FXR) is a therapeutic target of for the treatment of non-alcoholic fatty liver disease (NAFLD) owing to its regulatory role in lipid homeostasis. Schaftoside (SS) is a bioactive compound of Herba Desmodii Styracifolii , which has traditionally been used to treat hepatitis and cholelithiasis . However, the potential hepatoprotective effect of SS against NAFLD and the underlying mechanisms remain unknown. Aim of the study We investigated whether SS could improve NAFLD-induced liver injury by decreasing lipid accumulation via the activation of FXR signalling. Materials and methods In vivo , the effects of SS on high-fat diet (HFD)-induced lipid accumulation in the liver of mice were evaluated by serum biochemical parameters and histopathological analysis. In vitro , the intracellular triglyceride (TG) level and Oil Red O staining were used to evaluate the lipid removal ability of SS in Huh-7 cells or FXR knockout mouse primary hepatocytes (MPHs) induced by oleic acid (OA). Moreover, FXR/sterol regulatory element-binding protein 1 (SREBP1) mRNA and protein expression levels were detected. Results SS reduced HFD-induced lipid accumulation in the liver, as indicated by decreased aspartate aminotransferase (AST), cholesterol (Ch), and TG levels in serum and TG levels in liver tissue, and subsequently resulting in attenuation of liver histopathological injury. Gene expression profiles demonstrated that SS dose-dependently prevented HFD-induced decrease of FXR expression and inversely inhibited SREBP1 expression in the nucleus. Furthermore, SS significantly suppressed excessive TG accumulation and decreased intracellular TG level in Huh-7 cells or MPHs via the upregulation of FXR and inhibition of SREBP1 expression in the nucleus. Conclusion Our results suggest that SS ameliorates HFD-induced NAFLD by the decrease of lipid accumulation via the control of FXR-SREBP1 signalling.
研究领域:
药理学
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肝病学
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分子生物学
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民族药理学
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产品关联
DOI
PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
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2021
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IF 6.475
Chuang Zhu,Qi Guan,Chenwei Song,Lingyue Zhong,Xinwen Ding,Hui Zeng,Pan Nie,Lihua Song
Gut microbiota dysbiosis and oxidative stress may play important roles in the progression of nonalcoholic fatty liver disease (NAFLD). Fermented foods contain probiotics and other bioactive components that may improve gastrointestinal health and provide other health benefits. Here, we investigated the effect of Lactobacillus -fermented black barley on NAFLD rats. Adult Sprague Dawley rats were randomized into four groups: normal chow diet (NC), high-fat diet (HF), HF + fermented black barley treatment (HB) and HF + Lactobacillus treatment (HL). The rats in the HB and HL groups were continuously administered fermented black barley or Lactobacillus , respectively, for 12 weeks (1 mL/100 g·BW, containing 1 × 10 8 CFU/mL Lactobacillus ). Compared with the HF treatment, HB treatment effectively inhibited the increase in body weight, liver and abdominal fat indexes and hepatic lipids ( p < 0.01), increased hepatic SOD activity ( p < 0.05), decreased thiobarbituric acid reactive substances (TBARSs) ( p < 0.01) and improved liver function. Moreover, Lactobacillus -fermented black barley exhibited regulatory effect on high-fat diet-induced intestinal microbiota dysbiosis by increasing the relative microbiota abundance and diversity, increasing the relative abundance of Bacteroidetes , decreasing the Firmicutes/Bacteroidetes ratio, increasing the abundances of some intestinal probiotics (such as Akkermansia and Lactococcus ), and influencing some of the fecal metabolites related to hormones and lipid metabolism. The supplementation of fermented cereal food might be a new effective and safe preventive dietary strategy against NAFLD.
研究领域:
胃肠病学
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营养学
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微生物学
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肝病学
✓ 已验证
DOI
PubMed
高影响因子
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