TOXICOLOGY LETTERS
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2024
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IF 2.9
Yifei Shen,Jie Liu,Bingyi Yao,Yuanjin Zhang,Shengbo Huang,Chenmeizi Liang,Junze Huang,Yu Tang,Xin Wang
Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, which can cause serious complications and gradually increase the mortality rate. However, the effects of NAFLD on drug-metabolizing enzymes and transporters remain unclear, which may cause some confusion regarding patient medication. In this study, a NAFLD rat model was constructed by feeding rats with methionine and choline deficiency diets for 6 weeks, and the mRNA and protein levels of drug-metabolizing enzymes and transporter were analyzed by real-time fluorescent quantitative PCR and Western blot, respectively. The activity of drug-metabolizing enzymes was detected by cocktail methods. In the NAFLD rat model, the mRNA expression of phase I enzymes, phase II enzymes, and transporters decreased. At the protein level, only CYP1A1, CYP1B1, CYP2C11, and CYP2J3 presented a decrease. In addition, the activities of CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP3A2, UGT1A1, UGT1A3, UGT1A6, and UGT1A9 decreased. These changes may be caused by the alteration of FXR, HNF4α, LXRα, LXRβ, PXR, and RXR. In conclusion, NAFLD changes the expression and activity of hepatic drug-metabolizing enzymes and transporters in rats, which may affect drug metabolism and pharmacokinetics. In clinical medication, drug monitoring should be strengthened to avoid potential risks.
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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产品关联
DOI
PubMed
高影响因子
Food Frontiers
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2025
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IF 6.9
Xiaole Zhao,Bing Zheng,Tianxiang Ao,Jianhua Xie,Yi Chen,Hesham El-Seedi,Hairong Huang,Baoting Liu,Qiang Yu
Polygonatum cyrtonema polysaccharide (PCP-80%) is one of the major active ingredients in Polygonatum cyrtonema . By establishing the type 2 diabetes mellitus (T2DM) rat model and applying multi-omics analysis, the present study aimed to explore the potential mechanism of PCP-80% to alleviate T2DM in terms of the interactions between intestinal microbiota and their metabolites. The results suggested that PCP-80% effectively improve the blood glucose and lipids levels, enhance intestinal barrier function. In addition, PCP-80% restored gut microbiota disorders, increased the secretion of short-chain fatty acids (SCFAs), and enhanced bile acid (BA)-converting enzyme-rich microbiota abundance. Furthermore, PCP-80% intervention significantly ameliorated BA dysmetabolism while enhancing metabolic homeostasis in T2DM rats. These changes activated the G protein-coupled bile acid receptor 1 (TGR5) and farnesoid X receptor (FXR), triggering fibroblast growth factor 15 (FGF15) secretion to ameliorate T2DM-induced intestinal barrier dysfunction and glucose/lipid dysregulation. Mechanistically, PCP-80% exerted therapeutic effects through a microbiota-bile acid crosstalk axis, wherein gut microbiota remodeling enhanced bile acid metabolism and amplified TGR5/FXR-FGF15 signaling, ultimately restoring metabolic homeostasis in T2DM rats.
研究领域:
药理学
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微生物学
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内分泌学
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代谢组学
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糖尿病研究
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胃肠病学
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产品关联
DOI
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Guangyan Li,Tongshu Wang,Yixuan Xie,Lu He,Huan Liu,Hongying Chen,Hong Jiang,Taoguang Huo
Ethnopharmacological relevance Realgar is extensively utilized in both modern medicine and traditional Chinese medicine. Although it has therapeutic uses, realgar exhibits hepatotoxicity, and improper use can result in liver inflammation and injury. The disruption of bile acid (BA) homeostasis, identified as an initiating event in liver injury, has been observed in the livers of realgar-exposed mice. However, the relationship between realgar-induced BA homeostasis imbalance and liver inflammation remains to be elucidated. Aim of the study To investigate the relationship between hepatic BA homeostasis disorder and liver inflammation caused by realgar exposure in mice, as well as the role and potential mechanism of intestinal farnesoid X receptor (FXR) in realgar-induced liver inflammation. Methods A sub-chronic realgar exposure mouse model was established and subjected to interventions with an intestinal-restricted FXR agonist or inhibitor. Plasma hepatic enzyme activities and total bile acid (TBA) levels were quantified using spectrophotometry. Hepatic inflammatory cytokine levels were analyzed by ELISA or RT-qPCR. Histopathological evaluation of liver injury was performed using HE staining. F4/80 expression was assessed via immunohistochemistry (IHC). Western blot (WB) and IHC were employed to examine the expression of proteins involved in the FXR-FGF15 axis, and plasma FGF15 concentrations were determined by ELISA. The expression of proteins related to enterohepatic circulation and the NLRP3 inflammasome pathway were evaluated using WB. Ultra-performance liquid chromatography coupled with time-of-flight mass spectrometry (UPLC-TOF-MS) was utilized to analyze BA profiles in both ileal and hepatic tissues. Results Our findings demonstrate that realgar exposure induces changes in ileal BA composition and subsequent suppression of the FXR-FGF15 signaling axis in mice. This axis suppression promotes hepatic BA overproduction and disrupts BA homeostasis in the livers of realgar-exposed mice, particularly elevates the levels of taurochenodeoxycholic acid (TCDCA) and taurolithocholic acid (TLCA). In vitro studies revealed that both TCDCA and TLCA can directly activate the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in AML-12 cells, triggering pro-inflammatory cascades. Pharmacological activation of intestinal FXR effectively ameliorated realgar-induced hepatic inflammatory damage via restoring BA homeostasis and suppressing NLRP3 inflammasome activation. Conclusion Realgar exposure causes liver inflammatory injury by inducing BA-mediated NLRP3 inflammasome activation through down-regulating ileal FXR. Pharmacological activation of intestinal FXR alleviates realgar-induced liver inflammatory injury by restoring BA homeostasis and inhibiting BA-mediated NLRP3 inflammasome activation. These findings suggest that intestinal FXR may serve as a potential target for the prevention and treatment of realgar-induced liver injury.
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DOI
PubMed
高影响因子
Frontiers in Cell and Developmental Biology
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2021
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IF 6.684
Peijie Wu,Ling Qiao,Han Yu,Hui Ming,Chao Liu,Wenjun Wu,Baixue Li
Cholestasis is a kind of stressful syndrome along with liver toxicity, which has been demonstrated to be related to fibrosis, cirrhosis, even cholangiocellular or hepatocellular carcinomas. Cholestasis usually caused by the dysregulated metabolism of bile acids that possess high cellular toxicity and synthesized by cholesterol in the liver to undergo enterohepatic circulation. In cholestasis, the accumulation of bile acids in the liver causes biliary and hepatocyte injury, oxidative stress, and inflammation. The farnesoid X receptor (FXR) is regarded as a bile acid–activated receptor that regulates a network of genes involved in bile acid metabolism, providing a new therapeutic target to treat cholestatic diseases. Arbutin is a glycosylated hydroquinone isolated from medicinal plants in the genus Arctostaphylos , which has a variety of potentially pharmacological properties, such as anti-inflammatory, antihyperlipidemic, antiviral, antihyperglycemic, and antioxidant activity. However, the mechanistic contributions of arbutin to alleviate liver injury of cholestasis, especially its role on bile acid homeostasis via nuclear receptors, have not been fully elucidated. In this study, we demonstrate that arbutin has a protective effect on α -naphthylisothiocyanate–induced cholestasis via upregulation of the levels of FXR and downstream enzymes associated with bile acid homeostasis such as Bsep, Ntcp, and Sult2a1, as well as Ugt1a1. Furthermore, the regulation of these functional proteins related to bile acid homeostasis by arbutin could be alleviated by FXR silencing in L-02 cells. In conclusion, a protective effect could be supported by arbutin to alleviate ANIT-induced cholestatic liver toxicity, which was partly through the FXR pathway, suggesting arbutin may be a potential chemical molecule for the cholestatic disease.
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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毒理学
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产品关联
DOI
PubMed
高影响因子
BIOMEDICINE & PHARMACOTHERAPY
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2023
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IF 7.5
Xiongjie Sun,Yu Zhang,Gang Cheng,Tianxiang Zhu,Zhigang Zhang,Lei Xiong,Haiming Hu,Hongtao Liu
Ulcerative colitis (UC) has been confirmed as a disease with a high incidence and low cure rate worldwide. In severe cases, UC can develop into colon cancer. Modern research has confirmed that berberine (BBR) can treat UC by inhibiting the expressions of inflammatory factors. However, the contribution of gut microbiota and flora metabolites in treating UC with BBR remains unclear. In this study, the ameliorative effects of BBR on gut microbiota dysbiosis and flora metabolites were investigated in a dextran sodium sulfate (DSS)-induced UC rodent model. We found that BBR significantly improved the pathological phenotype, attenuated intestinal barrier disruption, and mitigated colonic inflammation in DSS mice. By 16 S rDNA sequencing, BBR alleviated gut microbiota dysbiosis in UC mice. Moreover, the gut microbiota depletion experiment confirmed that the therapeutic effect of BBR was inextricably correlated with the gut microbiota. Besides, the flora metabolites ( e.g. , short-chain fatty acids, bile acids, and 5-hydroxytryptamine) were studied using HPLC-MS. The results suggested that BBR ameliorated the bile acid imbalance induced by DSS in the liver and gut. Furthermore, BBR treatment repaired gut barrier damage. The above results revealed that BBR alleviated DSS-induced UC in mice by restoring the disturbed gut microbiota, elevating unconjugated and secondary bile acids in the gastrointestinal tract, and activating the FXR and TGR5 signal pathway. This study provides novel insights into the mechanism of BBR in treating UC.
研究领域:
药理学
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胃肠病学
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微生物学
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代谢组学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
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2025
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IF 4.8
Zhihui Li,Yanqiu Gu,Jianbo Yang,Shaozhan Wang,Shengnan Li,Panpan Chen,Ru Yao,Fangbin Liu,Ying Wang,Rong Wang,Yongfang Yuan
Introduction Polygonum multiflorum Thunb. (PM) is a representative traditional Chinese medicine (TCM) that exerts different effects in raw and processed forms. The hepatotoxicity of PM is markedly reduced after processing, whereas its hepatoprotective effects are enhanced. Purpose This study aimed to establish a novel comprehensive two-dimensional (2D) biochromatography system based on farnesoid X receptor (FXR), which is an important target in cholestatic liver injury (CLI), to investigate the material basis and mechanisms underlying the enhanced hepatoprotection and reduced hepatotoxicity of processed PM (P-PM). Methods A comprehensive 2D FXR biochromatography system was established by immobilizing FXR on 3-mercaptopropyltrimethoxysilane (MPTS)-modified silica gel. This system was used to identify the FXR-binding components in raw PM (R-PM) and P-PM. Molecular docking, surface plasmon resonance, and frontal affinity chromatography were used to validate the interactions. The hepatoprotective effects of emodin and physcion were assessed in α-naphthylisothiocyanate (ANIT)-induced CLI mouse models, and an FXR antagonist (Z-guggulsterone) rescue experiment was performed. The expression of FXR signaling-related proteins, including FXR, small heterodimer partner (SHP), bile salt export pump (BSEP), Na+-taurocholate cotransporting polypeptide (NTCP), and inflammatory cytokines, was assessed by Western blotting, real-time quantitative reverse transcription PCR, and immunofluorescence. Results The comprehensive 2D FXR biochromatography system successfully identified emodin and physcion as key FXR-binding components, with significantly increased content in P-PM. These components may contribute to the enhanced hepatoprotection and reduced hepatotoxicity of P-PM. In vivo , emodin and physcion alleviated ANIT-induced CLI, as evidenced by improved histopathological features and decreased serum levels of liver function markers. Mechanistically, both components upregulated the expression of FXR, BSEP, SHP, and NTCP while suppressing inflammatory cytokine expression. Their hepatoprotective effects and FXR-related upregulation could be disrupted by FXR antagonist Z-guggulsterone. These results suggest that emodin and physcion are key components contributing to the hepatoprotective effects of P-PM, likely through activation of the FXR signaling pathway and suppression of inflammation. Conclusion This study established a novel, efficient, rapid, and accurate comprehensive 2D FXR biochromatography system, which is suitable for screening targeted components in TCM, and can be extended to research on other TCMs.
研究领域:
生药学
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中医药学
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分子药理学
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天然产物化学
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肝脏疾病研究
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色谱分离技术
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
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2024
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IF 4.8
Yu Shen,Baorong Jiang,Zejia Hao,Chenchen Zhang,Zhan Zhang,Qian Wu,Lei Li,Ping Jiang
Both chromium picolinate (Cr-pic) and chromium trichloride (CrCl 3 ) were used as dietary supplements in agricultural products and foodstuffs. We found either these two forms of Cr(III) could ameliorate inflammation and cholestasis in DDC-induced primary sclerosing cholangitis (PSC) mice via regulating bile acid metabolism. Although two Cr(III) are able to alleviate hepatic inflammation by reducing the aggregation of macrophage, Cr-pic exhibiting superior efficacy in decreasing M1 macrophages. Two Cr(III) show inconsistent in regulating intestinal Fxr , but Cr-pic could active intestinal Fxr , promoting intestinal barrier repair. Additionally, both Cr-pic and CrCl 3 enhanced functional abundance of BSH enzymes involved in bile acid transformation, with Cr-pic seems to perturb the abundance of genus more than CrCl 3. In conclusion, this study highlights the efficacy of Cr-pic and CrCl 3 in mitigating inflammation and cholestasis in PSC, Cr-pic is expected superior than CrCl 3 to be supplement ingredient used in PSC treatment via regulating bile acid metabolism.
研究领域:
营养学
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胃肠病学
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药理学
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产品关联
DOI
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2021
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IF 4.36
Meiqi Wang,Fangle Liu,Yufeng Yao,Qiuyu Zhang,Zenghui Lu,Runjing Zhang,Changhui Liu,Chaozhan Lin,Chenchen Zhu
Ethnopharmacological relevance The well-known Chinese prescription, Xiaoyan Lidan Formula (XYLDF), possesses efficiency of heat-clearing, dampness-eliminating and jaundice-removing. It has long been used clinically for the treatment of hepatobiliary diseases due to intrahepatic cholestasis (IHC). However, the mechanism of XYLDF for its therapeutic effects remains elusive. Aim of the study The study aimed to explore the potential targets for liver protective mechanism of XYLDF based on network pharmacology and experimental assays in ANIT-induced cholestatic hepatic injury (CHI) in rats. Materials and methods On the basis of the 29 serum migrant compounds of XYLDF elucidated by UPLC-TOF-MS/MS, a network pharmacology approach was applied for the mechanism prediction. Systematic networks were constructed to identify potential molecular targets, biological processes, and signaling pathways. And the interactions between significantly potential targets and active compounds were simulated by molecular docking. For the mechanism validation, an ANIT-induced rat model was used to evaluate the effects of XYLDF on CHI according to serum biochemistry, bile flow rates, histopathological examination, and the gene and protein expression including enzymes related to synthesis, export, and import of bile acid in liver and ileum, and those of inflammatory cytokines, analyzed by RT-qPCR and WB. Results The results of network pharmacology research indicated TNF (TNF-α), RELA (NF-κB), NR1H4 (FXR), and ICAM1 (ICAM-1) to be the important potential targets of XYLDF for cholestatic liver injury, which are related to bile metabolism and NF-κB-mediated inflammatory signaling. And the molecular docking had pre-validated the prediction of network pharmacology, as the core active compounds of XYLDF had shown strong simulation binding affinity with FXR , followed by NF-κB, TNF-α, and ICAM-1. Meanwhile, the effects of XYLDF after oral administration on ANIT-induced CHI in rats exhibited the decreased levels of transaminases (ALT and AST), TBA, and TBIL in serum, raised bile flow rates, and markedly improved hepatic histopathology. Furthermore, consistent to the above targets prediction and molecular docking, XYLDF significantly up-regulated the expression of FXR, SHP, BSEP, and MRP2 , and down-regulated CYP7A1 and NTCP in liver, and promoted expression of IBABP and OSTα/β in ileum, suggesting the activation of FXR-mediated pathway referring to bile acid synthesis, transportation, and reabsorption. Moreover, the lower levels of TNF-α in plasma and liver, as well as the reduced hepatic gene and protein expression of NF-κB, TNF-α, and ICAM-1 after XYLDF treatment revealed the suppression of NF-κB-mediated inflammatory signaling pathway, as evidenced by the inhibition of nuclear translocation of NF-κB. Conclusions XYLDF exhibited an ameliorative liver protective effect on ANIT-induced cholestatic hepatic injury. The present study has confirmed its mechanism as activating the FXR-regulated bile acid pathway and inhibiting inflammation via the NF-κB signaling pathway.
研究领域:
药理学
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肝病学
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中医
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分子生物学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
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2023
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IF 7.9
Mei-Qi Wang,Kai-Hui Zhang,Fang-Le Liu,Rui Zhou,Yun Zeng,A-Li Chen,Yang Yu,Quan Xia,Chen-Chen Zhu,Chao-Zhan Lin
Background : Cholestatic liver diseases (CLD) comprise a variety of disorders of bile formation, which causes chronic exposure to bile acid (BA) in the liver generally and results in hepatotoxicity and progressive hepatobiliary injury. Wedelolactone (7-methoxy-5, 11, 12-trihydroxy-coumestan, WED), the natural active compound derived from Ecliptae Herba, has been reported with valuable bioactivity for liver protection. Nevertheless, the effect of WED on cholestatic liver injury (CLI) remains unexplored. Purpose : The present study aims to elucidate the protective effect of WED on Alpha-naphthylisothiocyanate (ANIT)-induced CLI mice, and to investigate its potential pharmacological mechanism. Methods : The anti-cholestasis and hepatoprotective effects of WED were evaluated in ANIT-induced CLI mice. Non-targeted metabolomics study combined with ingenuity pathway analysis (IPA) was used to explore the key mechanism of WED. The BA metabolic profile in enterohepatic circulation was analyzed to evaluate the effect of WED in regulating BA metabolism. Further, molecular dynamics (MD) simulation and cellular thermal shift assay (CETSA) were used to simulate and verify the targeting activation of WED on the Farnesoid X receptor (FXR). The core role of FXR in WED promoting BA transportation, and alleviating BA accumulation-induced hepatotoxicity was further evaluated in WT and FXR knockout mice or hepatocytes. Results : WED dose-dependently alleviated ANIT-induced cholestasis and liver injury in mice, and simultaneously suppressed the nuclear signaling pathway of factor-kappa B/nuclear factor-erythroid 2-related factor 2 (NF-κB/NRF2) to relieve inflammation and oxidative stress. At the metabolite level, WED improved the metabolic disorder in CLI mice focusing on the metabolism of BA, arachidonic acid, and glycerophospholipid, closely related to the process of BA regulation, inflammation, and oxidative damage. WED targeting activated FXR, which then transcribed its target genes, including the bile salt export pump (BSEP) and the BA transporter, which subsequently increased BA transportation to restore the damaged enterohepatic circulation of BA. Meanwhile, WED alleviated hepatic BA accumulation and protected the liver from BA-induced damage via NF-κB/NRF2 signaling pathway. Furthermore, FXR deficiency suppressed the protective effect of WED in vitro and in vivo . Conclusion : WED regulated BA metabolism and alleviated hepatic damage in cholestasis. It protected the liver according to adjusted BA transportation and relieved BA accumulation-related hepatotoxicity via FXR-bile acid-NF-κB/NRF2 axis. Our study provides novel insights that WED might be a promising strategy for cholestatic liver disease.
研究领域:
药理学
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肝病学
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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
CHEMICO-BIOLOGICAL INTERACTIONS
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2022
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IF 5.168
Moath Refat,Guoqiang Zhang,Abdulaziz Ahmed A.Saad,Salem Baldi,Fang Zheng,Xin'an Wu
Cholestasis is primarily caused by bile acid homeostasis dysregulation, resulting in retention, aggregation, and accumulation of the toxic cholate in the hepatocytes. Existing therapies for cholestasis are limited, demanding the urgent development of novel drugs. As a result, targeting FXR specifically promises a unique treatment strategy for cholestasis. The current study aims to evaluate the influence of 7, 8-dihydroxy-4-methyl coumarin (DMC) against alpha-naphthyl isothiocyanate (ANIT)-induced liver injury in mice. The “Computer-Aided Drug Design” (CADD) and molecular docking study anticipated that DMC would proficiently bind and activate the FXR. Accordingly, the hepatoprotective activity of DMC against ANIT-induced hepatotoxicity and cholestasis was investigated in ANIT-treated HepaRG cells and the ANIT-induced cholestatic mouse model. Outcomes indicated the protective effects of DMC against ANIT toxicity in HepaRG cells after 24 h of intervention and animals after seven days of treatment. DMC partially blocks ANIT-induced increases in serum markers of hepatocellular injury , liver and gall bladder enlargement , and hepatic necrosis . Western blotting revealed that DMC alleviates ANIT-induced hepatotoxicity and cholestasis via activating the FXR receptor and regulating CYP7A1 , the enzyme responsible for bile acid synthesis. DMC exhibited protective activity against cholestasis through activating FXR, suggesting it might be a promising strategy for preventing and treating cholestatic liver disease.
研究领域:
药理学
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肝病学
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分子生物学
·
药物发现
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2024
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IF 10.5
Qigu Yao,Beiduo Wang,Jiong Yu,Qiaoling Pan,Yingduo Yu,Xudong Feng,Wenyi Chen,Jinfeng Yang,Changyou Gao,Hongcui Cao
Primary sclerosing cholangitis (PSC) is a challenging cholestatic liver disease marked by progressive bile duct inflammation and fibrosis that has no FDA-approved therapy. Although obeticholic acid (OCA) has been sanctioned for PSC, its clinical utility in PSC is constrained by its potential hepatotoxicity. Here, we introduce a novel therapeutic construct consisting of OCA encapsulated within a reactive oxygen species (ROS)-responsive, biodegradable polymer, further cloaked with human placenta-derived mesenchymal stem cell (hP-MSC) membrane (MPPFTU@OCA). Using PSC patient-derived organoid models, we assessed its cellular uptake and cytotoxicity. Moreover, using a PSC mouse model induced by 3,5-diethoxycarbonyl-1,4-dihydro-collidine (DDC), we demonstrated that intravenous administration of MPPFTU@OCA not only improved cholestasis via the FXR-SHP pathway but also reduced macrophage infiltration and the accumulation of intracellular ROS, and alleviated mitochondria-induced apoptosis. Finally, we verified the ability of MPPFTU@OCA to inhibit mitochondrial ROS thereby alleviating apoptosis by measuring the mitochondrial adenosine triphosphate (ATP) concentration, ROS levels, and membrane potential (ΔΨm) using H 2 O 2 -stimulated PSC-derived organoids. These results illuminate the synergistic benefits of integrating an ROS-responsive biomimetic platform with OCA, offering a promising therapeutic avenue for PSC.
研究领域:
药理学
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肝病学
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纳米技术
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干细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Cell Reports
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2019
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IF 7.815
Kai Wang,Mingfang Liao,Nan Zhou,Li Bao,Ke Ma,Zhongyong Zheng,Yujing Wang,Chang Liu,Wenzhao Wang,Jun Wang,Shuang-Jiang Liu,Hongwei Liu
Summary We demonstrated the metabolic benefits of Parabacteroides distasonis (PD) on decreasing weight gain, hyperglycemia, and hepatic steatosis in ob/ob and high-fat diet (HFD)-fed mice. Treatment with live P. distasonis (LPD) dramatically altered the bile acid profile with elevated lithocholic acid (LCA) and ursodeoxycholic acid (UDCA) and increased the level of succinate in the gut. In vitro cultivation of PD demonstrated its capacity to transform bile acids and production of succinate. Succinate supplementation in the diet decreased hyperglycemia in ob/ob mice via the activation of intestinal gluconeogenesis (IGN). Gavage with a mixture of LCA and UDCA reduced hyperlipidemia by activating the FXR pathway and repairing gut barrier integrity. Co-treatment with succinate and LCA/UDCA mirrored the benefits of LPD. The binding target of succinate was identified as fructose-1,6-bisphosphatase, the rate-limiting enzyme in IGN. The succinate and secondary bile acids produced by P. distasonis played key roles in the modulation of host metabolism.
研究领域:
微生物学
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代谢学
·
胃肠病学
✓ 已验证
DOI
PubMed
高影响因子
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