PubMed

Related Articles Microbe participation in aroma production during soy sauce fermentation. J Biosci Bioeng. 2018 Jan 20;: Authors: Harada R, Yuzuki M, Ito K, Shiga K, Bamba T, Fukusaki E Abstract Soy sauce is a traditional Japanese fermented seasoning that contains various constituents such as amino acids, organic acids, and volatiles that are produced during the long fermentation process. Although studies regarding the correlation between microbes and aroma constituents have been performed, there are no reports about the influences of the microbial products, such as lactic acid, acetic acid, and ethanol, during fermentation. Because it is known that these compounds contribute to microbial growth and to changes in the constituent profile by altering the moromi environment, understanding the influence of these compounds is important. Metabolomics, the comprehensive study of low molecular weight metabolites, is a promising strategy for the deep understanding of constituent contributions to food characteristics. Therefore, the influences of microbes and their products such as lactic acid, acetic acid, and ethanol on aroma profiles were investigated using gas chromatography/mass spectrometry (GC/MS)-based metabolic profiling. The presence of aroma constituents influenced by microbes and chemically influenced by lactic acid, acetic acid, and ethanol were proposed. Most of the aroma constituents were not produced by adding ethanol alone, confirming the participation of yeast in aroma production. It was suggested that lactic acid bacterium relates to a key aromatic compound, 2,5-dimethyl-4-hydroxy-3(2H)-furanone. However, most of the measured aroma constituents changed similarly in both samples with lactic acid bacterium and acids. Thus, it was clear that the effect of lactic acid and acetic acid on the aroma profile was significant. PMID: 29366719 [PubMed - as supplied by publisher]

Related Articles Lipoprotein particle number and size distribution in apparently healthy spanish population according to sex and age, assessed by nuclear magnetic resonance. Atherosclerosis. 2017 Aug;263:e86 Authors: Gil Serret M, Ibarretxe D, Plana N, Correig X, Masana L, Amigó N PMID: 29366250 [PubMed - in process]

Related Articles Characterization of glycoprotein and lipoprotein profiles of rheumatoid arthritis (RA) patiens by 1H-nuclear magnetic resonance spectroscopy (1H-NMR). Atherosclerosis. 2017 Aug;263:e121 Authors: Fuertes Martín R, Amigó Grau N, Carles Vallvé J, Paredes S, Taverner D, Masana L, Correig Blanchar X PMID: 29365495 [PubMed - in process]

Related Articles Homeostatic control of metabolic and functional fitness of Treg cells by LKB1 signalling. Nature. 2017 08 31;548(7669):602-606 Authors: Yang K, Blanco DB, Neale G, Vogel P, Avila J, Clish CB, Wu C, Shrestha S, Rankin S, Long L, Kc A, Chi H Abstract Regulatory T cells (Treg cells) have a pivotal role in the establishment and maintenance of immunological self-tolerance and homeostasis. Transcriptional programming of regulatory mechanisms facilitates the functional activation of Treg cells in the prevention of diverse types of inflammatory responses. It remains unclear how Treg cells orchestrate their homeostasis and interplay with environmental signals. Here we show that liver kinase B1 (LKB1) programs the metabolic and functional fitness of Treg cells in the control of immune tolerance and homeostasis. Mice with a Treg-specific deletion of LKB1 developed a fatal inflammatory disease characterized by excessive TH2-type-dominant responses. LKB1 deficiency disrupted Treg cell survival and mitochondrial fitness and metabolism, but also induced aberrant expression of immune regulatory molecules including the negative co-receptor PD-1 and the TNF receptor superfamily proteins GITR and OX40. Unexpectedly, LKB1 function in Treg cells was independent of conventional AMPK signalling or the mTORC1-HIF-1α axis, but contributed to the activation of β-catenin signalling for the control of PD-1 and TNF receptor proteins. Blockade of PD-1 activity reinvigorated the ability of LKB1-deficient Treg cells to suppress TH2 responses and the interplay with dendritic cells primed by thymic stromal lymphopoietin. Thus, Treg cells use LKB1 signalling to coordinate their metabolic and immunological homeostasis and to prevent apoptotic and functional exhaustion, thereby orchestrating the balance between immunity and tolerance. PMID: 28847007 [PubMed - indexed for MEDLINE]

33 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 2018/01/25PubMed 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.

33 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 2018/01/25PubMed 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.

25 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 2018/01/24PubMed 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.

25 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 2018/01/24PubMed 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.

17 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 2018/01/23PubMed 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.

17 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 2018/01/23PubMed 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.

Metabolomics in Sepsis and Its Impact on Public Health. Public Health Genomics. 2018 Jan 19;: Authors: Evangelatos N, Bauer P, Reumann M, Satyamoorthy K, Lehrach H, Brand A Abstract Sepsis, with its often devastating consequences for patients and their families, remains a major public health concern that poses an increasing financial burden. Early resuscitation together with the elucidation of the biological pathways and pathophysiological mechanisms with the use of "-omics" technologies have started changing the clinical and research landscape in sepsis. Metabolomics (i.e., the study of the metabolome), an "-omics" technology further down in the "-omics" cascade between the genome and the phenome, could be particularly fruitful in sepsis research with the potential to alter the clinical practice. Apart from its benefit for the individual patient, metabolomics has an impact on public health that extends beyond its applications in medicine. In this review, we present recent developments in metabolomics research in sepsis, with a focus on pneumonia, and we discuss the impact of metabolomics on public health, with a focus on free/libre open source software. PMID: 29353273 [PubMed - as supplied by publisher]

NMR-based serum metabolomics study reveals a innovative diagnostic model for missed abortion. Biochem Biophys Res Commun. 2018 Jan 15;: Authors: Wu Z, Jin L, Zheng W, Zhang C, Zhang L, Chen Y, Guan J, Fei H Abstract A missed abortion (MA) is an in-utero death of the embryo or fetus before the 20th week of gestation with retained products of conception. In order to discover novel biomarkers for MA, a 1H NMR spectroscopy-based metabolomics approach was applied to detect human MA serum metabolic profiles. Serum samples were obtained from patients with MA (n = 15) and healthy controls (n = 9) for study. The NOESYPR1D spectrum combined with multi-variate pattern recognition analysis was used to cluster the groups and establish a disease-specific metabolites phenotype. Principal component analysis (PCA) and orthogonal partial least-squares discriminant analysis (OPLS-DA) models were capable of distinguishing MA patients from healthy subjects. The results revealed that 24 metabolites altered in MA patients compared with the control population. Metabolomic pathway analysis demonstrated that alanine, aspartate and glutamate metabolism, citrate cycle (TCA cycle), taurine and hypotaurine metabolism were significantly altered in MA. The results indicated that serum NMR-based metabolomic profiling method is sensitive and specific enough to distinguish MA and from healthy controls, this method could be developed as a clinically useful diagnostic tool for MA. The finding from the MA serum metabolic profiling shed a new light on further understanding of MA disease mechanisms. PMID: 29353036 [PubMed - as supplied by publisher]

Urine and plasma metabolomics study on potential hepatoxic biomarkers identification in rats induced by Gynura segetum. J Ethnopharmacol. 2018 Jan 15;: Authors: Shoubei Q, Haixia Z, Qianqian F, Fenxia Z, Jing W, Xiaobin J, Bin C Abstract ETHNOPHARMACOLOGICAL RELEVANCE: Gynura segetum (GS) is an herbal medicine containing Pyrrolizidine Alkaloids (PAs) that causes hepatic sinusoidal obstruction syndrome (HSOS). AIM OF THE STUDY: To discover potential biomarkers and metabolic mechanisms involved in the hepatotoxicity induced by GS. METHODS: SD rats were randomly divided into 4 groups including Saline, the decoction of GS high, medium and low dosage at dosages of 3.75g • kg-1, 7.5g • kg-1 and 15g • kg-1. A metabolomics approach using Ultraperformance Liquid Chromatography -Quadrupole-Time-of-Flight / Mass Spectrometry (UPLC-Q-TOF/MS) was developed to perform the plasma and urinary metabolic profiling analysis, and identified differential metabolites by comparing the saline control group and decoction of GS groups. RESULTS: The herbal was presented dosage-dependent led to ingravescence of hepatotoxicity after the rats were consecutively given with the decoction of GS at varied dosages. A total of 18 differential metabolites of decoction of GS-induced hepatotoxicity were identified, while 10 of them including arginine, proline, glutamate, creatine, valine, linoleic acid, arachidonic acid, sphinganine, phytosphingosine, and citric acid could be discovered in urine and plasma, and primarily involved in Amino acid metabolism, Lipids metabolism and Energy metabolism. CONCLUSIONS: The results suggested that the differential metabolites of arginine, creatine, valine, glutamine and citric acid were verified as potential markers of GS-induced hepatotoxicity via the regulation of multiple metabolic pathways primarily involving in Amino acids metabolism and Energy metabolism. PMID: 29353003 [PubMed - as supplied by publisher]

Fc gamma receptor binding profile of anti-citrullinated protein antibodies in immune complexes suggests a role for FcγRI in the pathogenesis of synovial inflammation. Clin Exp Rheumatol. 2018 Jan 15; Authors: Kempers AC, Nejadnik MR, Rombouts Y, Ioan-Facsinay A, van Oosterhout M, Jiskoot W, Huizinga TWJ, Toes REM, Scherer HU Abstract OBJECTIVES: Anti-citrullinated protein antibodies (ACPA) are highly specific for rheumatoid arthritis (RA). Here, we studied binding of ACPA-IgG immune complexes (IC) to individual Fc gamma receptors (FcγR) to identify potential effector mechanisms by which ACPA could contribute to RA pathogenesis. METHODS: ACPA-IgG1 and control IgG1(IgG1 depleted of ACPA-IgG1) were isolated from plasma and synovial fluid (SF) of RA patients by affinity chromatography using CCP2 peptides. Subsequently, IC were generated using fluorescently labelled F(ab')2 fragments against the F(ab')2 region of IgG, or by using citrullinated fibrinogen. IC were incubated with FcγR-transfected CHO cell lines or neutrophils from healthy donors. FcγR binding of IC was analysed by flow cytometry in the presence or absence of specific blocking antibodies. RESULTS: ACPA-IgG1 IC predominantly bound to FcγRI and FcγRIIIA on FcγR-transfected CHO cell lines, while much lower binding was observed to FcγRIIA and FcγRIIB. ACPA-IgG1 IC showed reduced binding to FcγRIIIA compared to control IgG1 IC, in line with enhanced ACPA-IgG1 Fc core-fucosylation. Neutrophils activated in vitro to induce de novo expression of FcγRI showed binding of ACPA-IgG IC, and blocking studies revealed that almost 30% of ACPA-IgG IC binding to activated neutrophils was mediated by FcγRI. CONCLUSIONS: Our studies show that ACPA-IgG1 IC bind predominately to activating FcγRI and FcγRIIIA, and highlight FcγRI expressed by activated neutrophils as relevant receptor for these IC. As neutrophils isolated from SF exhibit an activated state and express FcγRI in the synovial compartment, this IC-binding could contribute to driving disease pathogenesis in RA. PMID: 29352854 [PubMed - as supplied by publisher]

Related Articles Inhibitory effects of endogenous linoleic acid and glutaric acid on the renal glucuronidation of berberrubine in mice and on recombinant human UGT1A7, 1AB, and 1A9. Mol Pharmacol. 2018 Jan 19;: Authors: Yang N, Li S, Yan C, Sun R, He J, Xie Y, Peng Y, Wang G, Aa J Abstract Berberrubine (BRB) has a strong lipid-lowering effect and can be extensively metabolized into berberrubine-9-O-β-D-glucuronide (BRBG) in vivo. Recently, pharmacokinetics studies showed that the production of BRBG was significantly decreased in the urine of mice fed with a high fat diet (HFD), indicating a decreased glucuronidation capacity. Based on the UGT isoform identification, hepatic and renal microsomal incubation, glucuronidation was examined to suggest the metabolism of BRB in liver and kidneys. The results showed that the renal UGT activity for metabolizing BRB markedly decreased, which may be highly related to the decreased expression and activity of renal Ugt1a7c. Surprisingly, in vitro studies revealed neither BRB nor BRBG inhibited the renal UGT activity. By employing an integrated strategy of metabolomics and pharmacokinetics, we identified and confirmed for the first time the inhibitory effect of some potential endogenous molecules on the renal glucuronidation of C57BL/6J mice, such as glutaric acid and linoleic acid. By employing recombinant human UGTs, we found that glutaric acid and linoleic acid efficiently affect the activity of recombinant human UGT1A7, 1A9 and 1A8 at their normal or abnormal physiological levels in vivo. Glutaric acid (2 mM) markedly inhibited the activity of UGT1A7 by 89.4% and UGT1A9 by 32.8%. The inhibition rates reached 99.3% for UGT1A9, 48.3% for UGT1A7, and 46.8% for UGT1A8 with linoleic acid at 200 μM. It has been suggested that the endogenous molecules have the potential to affect the efficiency of glucuronidation, which might be a key factor contributing to individual differences in drug metabolism. PMID: 29351921 [PubMed - as supplied by publisher]

Related Articles EDC IMPACT: Molecular effects of developmental FM 550 exposure in Wistar rat placenta and fetal forebrain. Endocr Connect. 2018 Jan 19;: Authors: Baldwin KR, Horman B, Phillips AL, McRitchie SL, Watson S, Deese-Spruill J, Jima D, Sumner S, Stapleton H, Patisaul H Abstract Firemaster 550 (FM 550) is a flame retardant (FR) mixture that has become one of the most commonly used FRs in foam-based furniture and baby products. Human exposure to this commercial mixture, comprised of brominated and organophosphate components, is widespread. We have repeatedly shown that developmental exposure can lead to sex-specific behavioral effects in rats. Accruing evidence of endocrine disruption and potential neurotoxicity have raised concerns regarding the neurodevelopmental effects of FM 550 exposure, but the specific mechanisms of action remains unclear. Additionally, we observed significant, and in some cases sex-specific, accumulation of FM 550 in placental tissue following gestational exposure. Because the placenta is an important source of hormones and neurotransmitters for the developing brain, it may be a critical target of toxicity to consider in the context of developmental neurotoxicity. Using a mixture of targeted and exploratory approaches, the goal of the present study was to identify possible mechanisms of action in the developing forebrain and placenta. Wistar rat dams were orally exposed to FM 550 (0, 300, or 1,000 µg/day;) for 10 days during gestation and placenta and fetal forebrain tissue collected for analysis. In placenta, evidence of endocrine, inflammatory, and neurotransmitter signaling pathway disruption was identified. Notably, 5-HT turnover was reduced in placental tissue and fetal forebrains indicating that 5-HT signaling between the placenta and the embryonic brain may be disrupted. These findings demonstrate that environmental contaminants, like FM 550, have the potential to impact the developing brain by disrupting normal placental functions. PMID: 29351906 [PubMed - as supplied by publisher]

The serum metabolomics signature of Type 2 Diabetes is obscured in Alzheimer's Disease. Am J Physiol Endocrinol Metab. 2017 Dec 26;: Authors: Morris JK, Piccolo BD, Shankar K, Thyfault JP, Adams SH Abstract There is evidence for systemic metabolic impairment in Alzheimer's disease (AD), and Type 2 Diabetes (T2D) increases AD risk. Although studies analyzing blood metabolomics signatures have shown differences between cognitively healthy (CH) and AD subjects, these signatures have not been compared to individuals with T2D. We utilized untargeted analysis platforms (primary metabolism and complex lipids) to characterize the serum metabolome of 126 overnight fasted elderly subjects classified into 4 groups based upon AD status (CH or AD) and T2D status (Nondiabetic [ND] or T2D). Cognitive diagnosis groups were a priori weighted equally with T2D subjects. We hypothesized that AD subjects would display a similar metabolic profile to cognitively normal elderly individuals with T2D. However, partial least squared-discriminant analysis (PLS-DA) modelling resulted in poor classification across the four groups (< 50% classification accuracy of test subjects). Binary classification of AD vs. CH was poor, but binary classification of T2D vs. ND was good, providing >79.5% and >76.9% classification accuracy for held-out samples using primary metabolism and complex lipids, respectively). When modeling was limited to CH subjects, T2D discrimination improved for the primary metabolism platform (>89.5%) and remained accurate for complex lipids (>73% accuracy). Greater abundances of glucose, fatty acids (C20:2), and phosphatidylcholines and lower abundances of glycine, maleimide, octanol and tryptophan, cholesterol esters, phosphatidylcholines, and sphingomyelins were identified in CH subjects with T2D relative to those without T2D. In contrast, T2D was not accurately discriminated within AD subjects. Results herein suggest that AD may obscure the typical metabolic phenotype of T2D. PMID: 29351484 [PubMed - as supplied by publisher]

Heart in Lack of Oxygen? A Revisited Method to Improve Cardiac Performance Ex Vivo. Am J Physiol Heart Circ Physiol. 2017 Dec 15;: Authors: Ruiz M, Comtois P PMID: 29351474 [PubMed - as supplied by publisher]

Characterization of the proteome and lipidome profiles of human lung cells after low dose and chronic exposure to multiwalled carbon nanotubes. Nanotoxicology. 2018 Jan 19;:1-15 Authors: Phuyal S, Kasem M, Knittelfelder O, Sharma A, Fonseca DM, Vebraite V, Shaposhnikov S, Slupphaug G, Skaug V, Zienolddiny S Abstract The effects of long-term chronic exposure of human lung cells to multi-walled carbon nanotubes (MWCNT) and their impact upon cellular proteins and lipids were investigated. Since the lung is the major target organ, an in vitro normal bronchial epithelial cell line model was used. Additionally, to better mimic exposure to manufactured nanomaterials at occupational settings, cells were continuously exposed to two non-toxic and low doses of a MWCNT for 13-weeks. MWCNT-treatment increased ROS levels in cells without increasing oxidative DNA damage and resulted in differential expression of multiple anti- and pro-apoptotic proteins. The proteomic analysis of the MWCNT-exposed cells showed that among more than 5000 identified proteins; more than 200 were differentially expressed in the treated cells. Functional analyses revealed association of these differentially regulated proteins to cellular processes such as cell death and survival, cellular assembly, and organization. Similarly, shotgun lipidomic profiling revealed accumulation of multiple lipid classes. Our results indicate that long-term MWCNT-exposure of human normal lung cells at occupationally relevant low-doses may alter both the proteome and the lipidome profiles of the target epithelial cells in the lung. PMID: 29350075 [PubMed - as supplied by publisher]

Plasma metabolites associated with type 2 diabetes in a Swedish population: a case-control study nested in a prospective cohort. Diabetologia. 2018 Jan 18;: Authors: Shi L, Brunius C, Lehtonen M, Auriola S, Bergdahl IA, Rolandsson O, Hanhineva K, Landberg R Abstract AIMS/HYPOTHESIS: The aims of the present work were to identify plasma metabolites that predict future type 2 diabetes, to investigate the changes in identified metabolites among individuals who later did or did not develop type 2 diabetes over time, and to assess the extent to which inclusion of predictive metabolites could improve risk prediction. METHODS: We established a nested case-control study within the Swedish prospective population-based Västerbotten Intervention Programme cohort. Using untargeted liquid chromatography-MS metabolomics, we analysed plasma samples from 503 case-control pairs at baseline (a median time of 7 years prior to diagnosis) and samples from a subset of 187 case-control pairs at 10 years of follow-up. Discriminative metabolites between cases and controls at baseline were optimally selected using a multivariate data analysis pipeline adapted for large-scale metabolomics. Conditional logistic regression was used to assess associations between discriminative metabolites and future type 2 diabetes, adjusting for several known risk factors. Reproducibility of identified metabolites was estimated by intra-class correlation over the 10 year period among the subset of healthy participants; their systematic changes over time in relation to diagnosis among those who developed type 2 diabetes were investigated using mixed models. Risk prediction performance of models made from different predictors was evaluated using area under the receiver operating characteristic curve, discrimination improvement index and net reclassification index. RESULTS: We identified 46 predictive plasma metabolites of type 2 diabetes. Among novel findings, phosphatidylcholines (PCs) containing odd-chain fatty acids (C19:1 and C17:0) and 2-hydroxyethanesulfonate were associated with the likelihood of developing type 2 diabetes; we also confirmed previously identified predictive biomarkers. Identified metabolites strongly correlated with insulin resistance and/or beta cell dysfunction. Of 46 identified metabolites, 26 showed intermediate to high reproducibility among healthy individuals. Moreover, PCs with odd-chain fatty acids, branched-chain amino acids, 3-methyl-2-oxovaleric acid and glutamate changed over time along with disease progression among diabetes cases. Importantly, we found that a combination of five of the most robustly predictive metabolites significantly improved risk prediction if added to models with an a priori defined set of traditional risk factors, but only a marginal improvement was achieved when using models based on optimally selected traditional risk factors. CONCLUSIONS/INTERPRETATION: Predictive metabolites may improve understanding of the pathophysiology of type 2 diabetes and reflect disease progression, but they provide limited incremental value in risk prediction beyond optimal use of traditional risk factors. PMID: 29349498 [PubMed - as supplied by publisher]