PubMed

Dietary Mannan Oligosaccharides Modulate Gut Microbiota, Increase Fecal Bile Acid Excretion, and Decrease Plasma Cholesterol and Atherosclerosis Development. Mol Nutr Food Res. 2018 Apr 17;:e1700942 Authors: Hoving LR, Katiraei S, Heijink M, Pronk A, van der Wee-Pals L, Streefland T, Giera M, van Dijk KW, van Harmelen V Abstract SCOPE: Mannan oligosaccharides (MOS) have proven effective at improving growth performance, while also reducing hyperlipidemia and inflammation. As atherosclerosis is accelerated both by hyperlipidemia and inflammation, we aimed to determine the effect of dietary MOS on atherosclerosis development in hyperlipidemic ApoE*3-Leiden.CETP (E3L.CETP) mice, a well-established model for human-like lipoprotein metabolism. METHODS AND RESULTS: Female E3L.CETP mice were fed a high cholesterol diet, with or without 1% MOS for 14 weeks. MOS substantially decreased atherosclerotic lesions up to 54% as assessed in the valve area of the aortic root. In blood, IL-1RA, monocyte subtypes, lipids and bile acids (BAs) were not affected by MOS. Gut microbiota composition was determined using 16S rRNA gene sequencing and MOS increased the abundance of cecal Bacteroides Ovatus. MOS did not affect fecal excretion of cholesterol, but increased fecal BAs as well as butyrate in cecum as determined by gas-chromatography-mass-spectrometry. CONCLUSION: MOS decreased the onset of atherosclerosis development, via lowering of plasma cholesterol levels. These effects were accompanied by increased cecal butyrate and fecal excretion of BAs, presumably mediated via interactions of MOS with the gut microbiota. This article is protected by copyright. All rights reserved. PMID: 29665623 [PubMed - as supplied by publisher]

Lipidomic insight into cardiovascular diseases. Biochem Biophys Res Commun. 2018 Apr 14;: Authors: Kohno S, Keenan AL, Ntambi JM, Miyazaki M Abstract Cardiovascular disease is a primary cause of mortality worldwide. Therefore, it is of major interest to identify sensitive molecular markers that predict cardiovascular events and point to therapeutic strategies that will increase lifespans. Dysregulated lipid metabolism is recognized as an established risk factor in cardiovascular diseases. However, it is still largely unknown which specific lipid molecular species reflect cardiovascular risk. In addition, understanding the whole lipidome signature in vascular pathophysiology is challenging. Recent advancements of mass-spectrometry allow researchers to detect each individual lipid species from unbiased small samples. In this review, we update the current research on lipidomic approaches in cardiovascular diseases. PMID: 29665359 [PubMed - as supplied by publisher]

Sepsis Diagnostics in the Era of "Omics" Technologies. Prague Med Rep. 2018;119(1):9-29 Authors: Průcha M, Zazula R, Russwurm S Abstract Sepsis is a multifactorial clinical syndrome with an extremely dynamic clinical course and with high diverse clinical phenotype. Early diagnosis is crucial for the final clinical outcome. Previous studies have not identified a biomarker for the diagnosis of sepsis which would have sufficient sensitivity and specificity. Identification of the infectious agents or the use of molecular biology, next gene sequencing, has not brought significant benefit for the patient in terms of early diagnosis. Therefore, we are currently searching for biomarkers, through "omics" technologies with sufficient diagnostic specificity and sensitivity, able to predict the clinical course of the disease and the patient response to therapy. Current progress in the use of systems biology technologies brings us hope that by using big data from clinical trials such biomarkers will be found. PMID: 29665344 [PubMed - in process]

A prototypic small molecule database for bronchoalveolar lavage-based metabolomics. Sci Data. 2018 Apr 17;5:180060 Authors: Walmsley S, Cruickshank-Quinn C, Quinn K, Zhang X, Petrache I, Bowler RP, Reisdorph R, Reisdorph N Abstract The analysis of bronchoalveolar lavage fluid (BALF) using mass spectrometry-based metabolomics can provide insight into lung diseases, such as asthma. However, the important step of compound identification is hindered by the lack of a small molecule database that is specific for BALF. Here we describe prototypic, small molecule databases derived from human BALF samples (n=117). Human BALF was extracted into lipid and aqueous fractions and analyzed using liquid chromatography mass spectrometry. Following filtering to reduce contaminants and artifacts, the resulting BALF databases (BALF-DBs) contain 11,736 lipid and 658 aqueous compounds. Over 10% of these were found in 100% of samples. Testing the BALF-DBs using nested test sets produced a 99% match rate for lipids and 47% match rate for aqueous molecules. Searching an independent dataset resulted in 45% matching to the lipid BALF-DB compared to<25% when general databases are searched. The BALF-DBs are available for download from MetaboLights. Overall, the BALF-DBs can reduce false positives and improve confidence in compound identification compared to when general databases are used. PMID: 29664467 [PubMed - in process]

PPARα mediates the hepatoprotective effects of nutmeg. J Proteome Res. 2018 Apr 17;: Authors: Yang XN, Liu XM, Fang JH, Zhu X, Yang XW, Xiao XR, Huang JF, Gonzalez FJ, Li F Abstract Nutmeg is a traditional Chinese medicine used to treat gastrointestinal diseases. Some reports indicated that nutmeg has hepatoprotective activity. In this study, a thioacetamide (TAA)-induced acute liver injury model in mice was used to explore the mechanism of the protective effects of nutmeg extract (NME), including its major bioactive component myrislignan. The results indicated that NME could effectively protect TAA-induced liver damage as assessed by recovery of increased serum liver transaminases, decrease hepatic oxidative stress and lower hepatic inflammation. Metabolomics analysis further revealed that treatment with NME led to the recovery of a series of lipids including lysophosphatidylcholines that were decreased, and a lowering of acylcarnitines that were increased, in mouse plasma and liver after TAA exposure. Gene expression analysis demonstrated the hepatoprotective effect of NME was achieved by activation of the peroxisome proliferator-activated receptor alpha (PPARα), as well as the decrease of oxidative stress. NME could not protect from TAA-induced liver injury in Ppara-null mice, suggesting that its protective effect was dependent on PPARα. Myrislignan, a representative neolignan in nutmeg, showed potent protective activity against TAA-induced liver toxicity. These data demonstrate that nutmeg alleviates TAA-induced liver injury through the modulation of PPARα, and that the lignan compounds in nutmeg such as myrislignan partly contributed to this action. PMID: 29664296 [PubMed - as supplied by publisher]

Physiology, gene expression and metabolome of two wheat cultivars with contrasting submergence tolerance. Plant Cell Environ. 2018 Apr 17;: Authors: Herzog M, Fukao T, Winkel A, Konnerup D, Lamichhane S, Alpuerto JB, Hasler-Sheetal H, Pedersen O PMID: 29664146 [PubMed - as supplied by publisher]

Identification of Potential Biomarkers for Urine Metabolomics of Polycystic Ovary Syndrome Based on Gas Chromatography-Mass Spectrometry. Chin Med J (Engl). 2018 Apr 20;131(8):945-949 Authors: Zou Y, Zhu FF, Fang CY, Xiong XY, Li HY Abstract Background: Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder, and it's diagnosis is difficult. The aim of this study was to investigate the metabolic profiles of PCOS patients by analyzing urine samples and identify useful biomarkers for diagnosis of PCOS. Methods: This study was carried out in the Department of Obstetrics and Gynecology of the Maternal and Child Health Hospital of Hunan Province from December 2014 to July 2016. In this study, the urine samples of 21 women with PCOS and 16 healthy controls were assessed through gas chromatography-mass spectrometry to investigate the urine metabolite characteristics of PCOS and identify useful biomarkers for the diagnosis of this disorder. The Student's t-test and rank sum test were applied to validate the statistical significance of the between the two groups. Results: In total, 35 urine metabolites were found to be significantly different between the PCOS patients and the controls. In particular, a significant increase in the levels of lactose (10.01 [0,13.99] mmol/mol creatinine vs. 2.35 [0.16, 3.26] mmol/mol creatinine, P = 0.042), stearic acid (2.35 [1.47, 3.14] mmol/mol creatinine vs. 0.05 [0, 0.14] mmol/mol creatinine, P < 0.001), and palmitic acid (2.13 [1.07, 2.79] mmol/mol creatinine vs. 0 [0, 0] mmol/mol creatinine, P < 0.001) and a decrease in the levels of succinic acid (0 [0, 0] mmol/mol creatinine vs. 38.94 [4.16, 51.30] mmol/mol creatinine, P < 0.001) were found in the PCOS patients compared with the controls. It was possible to cluster the PCOS patients and the healthy controls into two distinct regions based on a principal component analysis model. Of the differentially expressed metabolites, four compounds, including stearic acid, palmitic acid, benzoylglycine, and threonine, were selected as potential biomarkers. Conclusions: This study offers new insight into the pathogenesis of PCOS, and the discriminating urine metabolites may provide a prospect for the diagnosis of PCOS. PMID: 29664055 [PubMed - in process]

Related Articles Hepatocellular Carcinoma-associated Protein TD26 Interacts and Enhances SREBP1 Activity to Promote Tumor Cell Proliferation and Growth. Hepatology. 2018 Apr 16;: Authors: Wang C, Tong Y, Wen Y, Cai J, Guo H, Huang L, Xu M, Feng M, Chen X, Zhang J, Wu H, Kong X, Xia Q Abstract Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Increased lipogenesis has been reported to play a critical role in HCC progression. However, the underlying mechanism contributing to lipogenesis increase in HCC remains elusive. Here, we show that hepatocellular carcinoma-associated protein TD26 (TD26) was highly expressed in HCC tumor tissues compared to matched normal tissues. From the clinicopathologic analyses of two independent HCC cohorts, we demonstrate that TD26 expression was positively correlated with tumor size and was an independent predictor of overall survival (OS) and recurrence free survival (RFS) in HCC patients. Our metabolomics assays demonstrate that TD26 had no effect on glycometabolism but significantly increased lipogenesis in HCC cells. In addition, our functional assays indicate that TD26 promoted HCC cell proliferation and tumor growth. We further demonstrate that TD26-mediated increase in lipogenesis and tumor cell proliferation was SREBP1-dependent. Mechanistically, we demonstrate that, through its C-terminus (amino acids from 121 to 198), TD26 interacted with the truncated nuclear SREBP1 form (nSREBP1) but not the SREBP1 full-length (flSREBP1) to block AMPK-mediated inhibition on SREBP1 activity, resulting in increased lipogenesis, elevated tumor cell proliferation and enhanced tumor progression. Therefore, we propose that TD26 is a novel positive regulator on SREBP1 transactivity and the interaction between TD26 and SREBP1 can serve as a potential therapeutic target for HCC treatment. This article is protected by copyright. All rights reserved. PMID: 29663480 [PubMed - as supplied by publisher]

Related Articles The role of the Human Metabolome Database in inborn errors of metabolism. J Inherit Metab Dis. 2018 Apr 16;: Authors: Mandal R, Chamot D, Wishart DS Abstract Metabolomics holds considerable promise to advance our understanding of human disease, including our understanding of inborn errors of metabolism (IEM). The application of metabolomics in IEM research has already led to the discovery of several novel IEMs and the identification of novel IEM biomarkers. However, with hundreds of known IEMs and more than 700 associated IEM metabolites, it is becoming increasingly challenging for clinical researchers to keep track of IEMs, their associated metabolites, and their corresponding metabolic mechanisms. Furthermore, when using metabolomics to assist in IEM biomarker discovery or even in IEM diagnosis, it is becoming much more difficult to properly identify metabolites from the complex NMR and MS spectra collected from IEM patients. To that end, comprehensive, open access metabolite databases that provide up-to-date referential information about metabolites, metabolic pathways, normal/abnormal metabolite concentrations, and reference NMR or MS spectra for compound identification are essential. Over the last few years, a number of compound databases, including the Human Metabolome Database (HMDB), have been developed to address these challenges. First described in 2007, the HMDB is now the world's largest and most comprehensive metabolomic resource for human metabolic studies. The latest release of the HMDB contains 114,100 metabolite entries (with 247 being relevant to IEMs), thousands of metabolite concentrations (with 600 being relevant to IEMs), and ~33,000 metabolic and disease-associated pathways (with 202 being relevant to IEMs). Here we provide a summary of the HMDB and offer some guidance on how it can be used in metabolomic studies of IEMs. PMID: 29663269 [PubMed - as supplied by publisher]

Related Articles Comparative Analysis of the Microbiota Between Sheep Rumen and Rabbit Cecum Provides New Insight Into Their Differential Methane Production. Front Microbiol. 2018;9:575 Authors: Mi L, Yang B, Hu X, Luo Y, Liu J, Yu Z, Wang J Abstract The rumen and the hindgut represent two different fermentation organs in herbivorous mammals, with the former producing much more methane than the latter. The objective of this study was to elucidate the microbial underpinning of such differential methane outputs between these two digestive organs. Methane production was measured from 5 adult sheep and 15 adult rabbits, both of which were placed in open-circuit respiratory chambers and fed the same diet (alfalfa hay). The sheep produced more methane than the rabbits per unit of metabolic body weight, digestible neutral detergent fiber, and acid detergent fiber. pH in the sheep rumen was more than 1 unit higher than that in the rabbit cecum. The acetate to propionate ratio in the rabbit cecum was more than threefold greater than that in the sheep rumen. Comparative analysis of 16S rRNA gene amplicon libraries revealed distinct microbiota between the rumen of sheep and the cecum of rabbits. Hydrogen-producing fibrolytic bacteria, especially Butyrivibrio, Succiniclastium, Mogibacterium, Prevotella, and Christensenellaceae, were more predominant in the sheep rumen, whereas non-hydrogen producing fibrolytic bacteria, such as Bacteroides, were more predominant in the rabbit cecum. The rabbit cecum had a greater predominance of acetogens, such as those in the genus Blautia, order Clostridiales, and family Ruminococcaceae. The differences in the occurrence of hydrogen-metabolizing bacteria probably explain much of the differential methane outputs from the rumen and the cecum. Future research using metatranscriptomics and metabolomics shall help confirm this premise and understand the factors that shape the differential microbiota between the two digestive organs. Furthermore, our present study strongly suggests the presence of new fibrolytic bacteria in the rabbit cecum, which may explain the stronger fibrolytic activities therein. PMID: 29662480 [PubMed]

Related Articles Initial Metabolic Profiles Are Associated with 7-Day Survival among Infants Born at 22-25 Weeks of Gestation. J Pediatr. 2018 Apr 13;: Authors: Oltman SP, Rogers EE, Baer RJ, Anderson JG, Steurer MA, Pantell MS, Partridge JC, Rand L, Ryckman KK, Jelliffe-Pawlowski LL Abstract OBJECTIVE: To evaluate the association between early metabolic profiles combined with infant characteristics and survival past 7 days of age in infants born at 22-25 weeks of gestation. STUDY DESIGN: This nested case-control consisted of 465 singleton live births in California from 2005 to 2011 at 22-25 weeks of gestation. All infants had newborn metabolic screening data available. Data included linked birth certificate and mother and infant hospital discharge records. Mortality was derived from linked death certificates and death discharge information. Each death within 7 days was matched to 4 surviving controls by gestational age and birth weight z score category, leaving 93 cases and 372 controls. The association between explanatory variables and 7-day survival was modeled via stepwise logistic regression. Infant characteristics, 42 metabolites, and 12 metabolite ratios were considered for model inclusion. Model performance was assessed via area under the curve. RESULTS: The final model included 1 characteristic and 11 metabolites. The model demonstrated a strong association between metabolic patterns and infant survival (area under the curve [AUC] 0.885, 95% CI 0.851-0.920). Furthermore, a model with just the selected metabolites performed better (AUC 0.879, 95% CI 0.841-0.916) than a model with multiple clinical characteristics (AUC 0.685, 95% CI 0.627-0.742). CONCLUSIONS: Use of metabolomics significantly strengthens the association with 7-day survival in infants born extremely premature. Physicians may be able to use metabolic profiles at birth to refine mortality risks and inform postnatal counseling for infants born at <26 weeks of gestation. PMID: 29661562 [PubMed - as supplied by publisher]

Related Articles Autophagy couteracts weight gain, lipotoxicity and pancreatic β-cell death upon hypercaloric pro-diabetic regimens. Cell Death Dis. 2017 Aug 03;8(8):e2970 Authors: Fernández ÁF, Bárcena C, Martínez-García GG, Tamargo-Gómez I, Suárez MF, Pietrocola F, Castoldi F, Esteban L, Sierra-Filardi E, Boya P, López-Otín C, Kroemer G, Mariño G Abstract In the last years, autophagy has been revealed as an essential pathway for multiple biological processes and physiological functions. As a catabolic route, autophagy regulation by nutrient availability has been evolutionarily conserved from yeast to mammals. On one hand, autophagy induction by starvation is associated with a significant loss in body weight in mice. Here, we demonstrate that both genetic and pharmacological inhibition of the autophagy process compromise weight loss induced by starvation. Moreover, autophagic potential also impacts on weight gain induced by distinct hypercaloric regimens. Atg4b-deficient mice, which show limited autophagic competence, exhibit a major increase in body weight in response to distinct obesity-associated metabolic challenges. This response is characterized by the presence of larger adipocytes in visceral fat tissue, increased hepatic steatosis, as well as reduced glucose tolerance and attenuated insulin responses. Similarly, autophagy-deficient mice are more vulnerable to experimentally induced type-I diabetes, showing an increased susceptibility to acute streptozotocin administration. Notably, pharmacological stimulation of autophagy in wild-type mice by spermidine reduced both weight gain and obesity-associated alterations upon hypercaloric regimens. Altogether, these results indicate that systemic autophagic activity influences the resilience of the organism to weight gain induced by high-calorie diets, as well as to the obesity-associated features of both type-1 and type-2 diabetes. PMID: 28771229 [PubMed - indexed for MEDLINE]

Related Articles mTORC1 Regulates Mitochondrial Integrated Stress Response and Mitochondrial Myopathy Progression. Cell Metab. 2017 Aug 01;26(2):419-428.e5 Authors: Khan NA, Nikkanen J, Yatsuga S, Jackson C, Wang L, Pradhan S, Kivelä R, Pessia A, Velagapudi V, Suomalainen A Abstract Mitochondrial dysfunction elicits various stress responses in different model systems, but how these responses relate to each other and contribute to mitochondrial disease has remained unclear. Mitochondrial myopathy (MM) is the most common manifestation of adult-onset mitochondrial disease and shows a multifaceted tissue-specific stress response: (1) transcriptional response, including metabolic cytokines FGF21 and GDF15; (2) remodeling of one-carbon metabolism; and (3) mitochondrial unfolded protein response. We show that these processes are part of one integrated mitochondrial stress response (ISRmt), which is controlled by mTORC1 in muscle. mTORC1 inhibition by rapamycin downregulated all components of ISRmt, improved all MM hallmarks, and reversed the progression of even late-stage MM, without inducing mitochondrial biogenesis. Our evidence suggests that (1) chronic upregulation of anabolic pathways contributes to MM progression, (2) long-term induction of ISRmt is not protective for muscle, and (3) rapamycin treatment trials should be considered for adult-type MM with raised FGF21. PMID: 28768179 [PubMed - indexed for MEDLINE]

18 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2018/04/17PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

18 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2018/04/17PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

30 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2018/04/16PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

23 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2018/04/15PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Related Articles A review of the pharmaceutical exposome in aquatic fauna. Environ Pollut. 2018 Apr 10;239:129-146 Authors: Miller TH, Bury NR, Owen SF, MacRae JI, Barron LP Abstract Pharmaceuticals have been considered 'contaminants of emerging concern' for more than 20 years. In that time, many laboratory studies have sought to identify hazard and assess risk in the aquatic environment, whilst field studies have searched for targeted candidates and occurrence trends using advanced analytical techniques. However, a lack of a systematic approach to the detection and quantification of pharmaceuticals has provided a fragmented literature of serendipitous approaches. Evaluation of the extent of the risk for the plethora of human and veterinary pharmaceuticals available requires the reliable measurement of trace levels of contaminants across different environmental compartments (water, sediment, biota - of which biota has been largely neglected). The focus on pharmaceutical concentrations in surface waters and other exposure media have therefore limited both the characterisation of the exposome in aquatic wildlife and the understanding of cause and effect relationships. Here, we compile the current analytical approaches and available occurrence and accumulation data in biota to review the current state of research in the field. Our analysis provides evidence in support of the 'Matthew Effect' and raises critical questions about the use of targeted analyte lists for biomonitoring. We provide six recommendations to stimulate and improve future research avenues. PMID: 29653304 [PubMed - as supplied by publisher]

Related Articles Effects of glaucocalyxin A on human liver cancer cells as revealed by GC/MS- and LC/MS-based metabolic profiling. Anal Bioanal Chem. 2018 Apr 13;: Authors: Liu Y, Lu S, Zhao L, Dong X, Zhu Z, Jin Y, Chen H, Lu F, Hong Z, Chai Y Abstract Studies have documented the potential antitumor activities of glaucocalyxin A (GLA), an ent-kaurene diterpenoid isolated from Rabdosia japonica. However, the metabolic mechanism underlying the antitumor activity of GLA remains largely unknown. The effects of GLA on the metabolome of human liver cancer cells using GC/MS- and LC/MS-based metabolic profiling have been investigated. An untargeted metabolomics approach in conjunction with orthogonal projection to latent structures-discriminant analysis (OPLS-DA) has been developed to characterize the metabolic modifications induced by GLA treatment in human hepatoma cell line SMMC7721. Results demonstrated that cells cultured in the presence or absence of GLA displayed different metabolic profiles: the treatment induced an increased purine metabolism, pyrimidine metabolism, and sphingolipid metabolism and a decreased amino acid metabolism. At the same time, GLA treatment induced cell apoptosis and cell cycle arrested at G2/M phase in a dose-dependent manner. In addition, two representative apoptosis-inducing cytotoxic agents were selected as positive control drugs to validate the reasonableness and accuracy of our metabolomic investigation on GLA. The study displayed a systemic metabolic alteration induced by GLA treatment, showing the impaired physiological activity of SMMC7721 cells, which also indicated anti-proliferative and apoptotic effects of GLA. In the meantime, GC/MS- and LC/MS-based metabolomics applied to cell culture enhanced our current understanding of the metabolic response to GLA treatment and its mechanism; such an approach could be transferred to study the mechanism of other anticancer drugs. Graphical abstract A systemic metabolic alteration induced by glaucocalyxin A (GLA) treatment of SMMC-7721 cells. PMID: 29651531 [PubMed - as supplied by publisher]

Related Articles Antiseptic Activity of Ethnomedicinal Xuebijing Revealed by the Metabolomics Analysis Using UHPLC-Q-Orbitrap HRMS. Front Pharmacol. 2018;9:300 Authors: Zuo L, Zhou L, Xu T, Li Z, Liu L, Shi Y, Kang J, Gao G, Du S, Sun Z, Zhang X Abstract Xuebijing (XBJ) injection is an ethnomedicinal formula that has been widely used in the therapy of sepsis in China. However, the underlying theraputic mechanisms remain uninvestigated. In this research, a metabolomic method based on UHPLC-Q-Orbitrap HRMS was applied to make a holistic evaluation of XBJ on septic rats which were induced by the classical cecal ligation and puncture (CLP) operation. The plasma metabolic changes were profiled and evaluated by multivariate analytical (MVA) methods. In the results, a total of 41 differential metabolites were identified between CLP-operated group and sham-operated group, which were mainly involved in amino acid metabolism and lipid metabolism. After pathway analysis, it was finally discovered that the majority of the influenced metabolic pathways caused by sepsis mainly involved in energy metabolism, oxidative stress, and inflammation metabolism. When intervened by XBJ injection, 32 of the 41 disordered metabolites had been adjusted in reverse, which suggested that XBJ could mediate the abnormal metabolic pathways synergistically. In conclusion, the present study systematically investigated the efficacy and its underlying therapeutic mechanisms of XBJ on sepsis, while offering a new insight for the subsequent relevant exploration of other Chinese medicine at the same time. PMID: 29651245 [PubMed]