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3,861 results for “Glucose”
FIGURE 3 in Dimethyl acetamide and dimethyl sulfoxide associated at glucose and egg yolk for cryopreservation of Pseudoplatystoma corruscans semen
FIGURE 3 | Morphological characteristics of the Pseudoplatystoma corruscans sperm. A and B, normal spermatozoa; C and D, sperm with malformations. Legends: h1, width; h2, length; mp, intermediate part; #, sperm without the flagellum; c, curled tail; rmp, reduced middle piece. Scale bars; A and C = 20 µm; B and D = 5 µm.
Polysome profile glucose beta-cells
<p>Polysome profile analysis of human pancreatic beta-cells exposure to glucose</p> <p>A human pancreatic beta cell line (betaH2) was exposed to glucose after starvation.<br> Total RNA was collected for a bulk RNA-seq analysis. Three biological repeats were produced for each of the the low and high glucose conditions resulting in to 6 sequence (fastq) files.<br> Three different mRNA-ribosomal fractions were selected from a sucrose gradient corresponding to single ribosomes (monosomes), light ribosomes (2-4) and heavy ribosomes (5 and more).<br> Three biological repeats were produced for each fraction and for the two conditions (low and high glucose) resulting to 18 different (fastq) sequenced files.</p> <p>In total the study consists of 24 submitted fastq files, 6 corresponding to total RNA from two conditions (three replicates) and 18 corresponding to polysome profile, 3 fractions times two conditions times 3 replicates.</p> <p>All 24 *.fastq.gz files are available in the reads_PolysomeProfile_RNAseq_BetaCells.tar archive.</p> <p>In addition to the raw reads we provide the processed data:<br> The raw counts table ( countsTOTALS_CodingGenes.tsv) and the Transcripts Per Million table (TPMs) (polysomeProfile_TPM_proteinCoding.csv) files of the data produced from the polysome profile and RNA-seq experiments described in the experimental design that can be found in:<br> https://github.com/parisepigenetics/Translatome_Bcells_glucose</p>
Simultaneous dynamic glucose-enhanced (DGE) MRI and fiber photometry measurements of glucose in the healthy mouse brain
<p>This dataset was acquired for the DGE and fiber photometry study published in NeuroImage ( <a href="https://doi.org/10.1016/j.neuroimage.2022.119762">https://doi.org/10.1016/j.neuroimage.2022.119762</a>).<br> Comprises of three datasets: DGE MRI, fiber photometry and two-photon microscopy.</p>
Glucose and Non-Invasive Brain Stimulation
ClinicalTrials.gov study NCT04031404. IPD Sharing: YES. Countries: 1. Publications: 1.
Development of Continuous Glucose Monitoring System Cohort for Personalized Diabetes Prevention and Management Platform
ClinicalTrials.gov study NCT04369833. IPD Sharing: NO. Countries: 1. Publications: 11.
Effects of Pioglitazone on Insulin and Glucose Metabolism in Women With Polycystic Ovary Syndrome (PCOS)
ClinicalTrials.gov study NCT00868140. IPD Sharing: NO. Countries: 2. Publications: 1.
Oral Amino Acid Nutrition to Improve Glucose Excursions in PCOS
ClinicalTrials.gov study NCT03717935. IPD Sharing: NO. Countries: 1. Publications: 0.
Three Approaches to Glucose Monitoring in Non-insulin Treated Diabetes
ClinicalTrials.gov study NCT02033499. IPD Sharing: YES. Countries: 1. Publications: 10.
Comparison of Glucose Values and Variability Between TOUJEO and TRESIBA During Continuous Glucose Monitoring in Type 1 Diabetes Patients
ClinicalTrials.gov study NCT04075513. IPD Sharing: YES. Countries: 7. Publications: 1.
Crystal structure of glucose isomerase from S. rubiginosus soaked with EDTA for 1min
<p>Data: Diffraction images of crystal structure of glucose isomerase soaked with EDTA for 1min</p> <p>Experimental method: X-ray crystallography.</p> <p>Data collection: 11C beamline, Pohang Accelerator Laboratory</p>
VTR case studies datasets: myoglobin against hemoglobin, RBDs of SARS-CoV-1 vs. SARS-CoV-2, and glucose-tolerant vs. non-tolerant β-glucosidases
<p>Description of the four files:</p> <ol> <li><strong>contacts.xlsx</strong> <ul> <li>List of detected contacts for the three case studies</li> </ul> </li> <li><strong>pymol_files_case_study_1.zip</strong> <ul> <li>Contains files in PDB format of the analyzed structures, and files in PML format used to display visualizations in the PyMOL tool for the case study 1: comparison between contacts of myoglobin against hemoglobin</li> </ul> </li> <li><strong>pymol_files_case_study_2.zip</strong> <ul> <li>Contains files in PDB format of the analyzed structures, and files in PML format used to display visualizations in the PyMOL tool for the case study 2: comparison between contacts of RBDs of SARS-CoV-1 vs. SARS-CoV-2 both complexed with the cell receptor ACE2</li> </ul> </li> <li><strong>pymol_files_case_study_3.zip</strong> <ul> <li>Contains files in PDB format of the analyzed structures, and files in PML format used to display visualizations in the PyMOL tool for the case study 3: comparison between contacts of glucose-tolerant vs. non-tolerant β-glucosidases </li> </ul> </li> </ol>
Data from: Safety of single low-dose primaquine in glucose-6-phosphate dehydrogenase deficient falciparum-infected African males: two open-label, randomized, safety trials
Background: Primaquine (PQ) actively clears mature Plasmodium falciparum gametocytes but in glucose-6-phosphate dehydrogenase deficient (G6PDd) individuals can cause hemolysis. We assessed the safety of low-dose PQ in combination with artemether-lumefantrine (AL) or dihydroartemisinin-piperaquine (DP) in G6PDd African males with asymptomatic P. falciparum malaria. Methods and findings: In Burkina Faso, G6PDd adult males were randomized to treatment with AL alone (n = 10) or with PQ at 0.25 (n = 20) or 0.40 mg/kg (n = 20) dosage; G6PD-normal males received AL plus 0.25 (n = 10) or 0.40 mg/kg (n = 10) PQ. In The Gambia, G6PDd adult males and boys received DP alone (n = 10) or with 0.25 mg/kg PQ (n = 20); G6PD-normal males received DP plus 0.25 (n = 10) or 0.40 mg/kg (n = 10) PQ. The primary study endpoint was change in hemoglobin concentration during the 28-day follow-up. Cytochrome P-450 isoenzyme 2D6 (CYP2D6) metabolizer status, gametocyte carriage, haptoglobin, lactate dehydrogenase levels and reticulocyte counts were also determined. In Burkina Faso, the mean maximum absolute change in hemoglobin was -2.13 g/dL (95% confidence interval [CI], -2.78, -1.49) in G6PDd individuals randomized to 0.25 PQ mg/kg and -2.29 g/dL (95% CI, -2.79, -1.79) in those receiving 0.40 PQ mg/kg. In The Gambia, the mean maximum absolute change in hemoglobin concentration was -1.83 g/dL (95% CI, -2.19, -1.47) in G6PDd individuals receiving 0.25 PQ mg/kg. After adjustment for baseline concentrations, hemoglobin reductions in G6PDd individuals in Burkina Faso were more pronounced compared to those in G6PD-normal individuals receiving the same PQ doses (P = 0.062 and P = 0.022, respectively). Hemoglobin levels normalized during follow-up. Abnormal haptoglobin and lactate dehydrogenase levels provided additional evidence of mild transient hemolysis post-PQ. Conclusions: Single low-dose PQ in combination with AL and DP was associated with mild and transient reductions in hemoglobin. None of the study participants developed moderate or severe anemia; there were no severe adverse events. This indicates that single low-dose PQ is safe in G6PDd African males when used with artemisinin-based combination therapy.
Volumetric properties of dilute (d-glucose + H2O) solutions at temperatures from (293.15 to 433.15) K and pressures from (0.10 to 50.00) MPa
<p>The densities of aqueous solutions of D-glucose were measure at temperatures from (293.15 to 433.15) K and pressures from (0.10 to 50.00) MPa using a vibrating-tube densimeter. Apparent molar volumes <i>V</i><sub>φ,m</sub> and partial molar volumes at infinite dilution <i>V</i><sup>∞</sup> were calculated from the experimental results. <i>V</i><sup>∞</sup> increases as temperature increases and varies linearly with temperature above ~300 K. In addition, <i>V</i><sup>∞ </sup>does not vary as a function of pressure up to 50.0 MPa. Comparison of these results with previous studies indicate excellent agreement and significantly extend the experimental database for aqueous solutions of D-glucose to elevated temperatures and pressures. </p>
Data from: Gut microbiota composition and functionality are associated with REM sleep duration and continuous glucose levels
<p><span><strong>Context</strong>:</span><span> Sleep disruption is associated with poorer glucose metabolic control and altered gut microbiota in animal models.</span></p> <p><span><strong>Objective</strong>:</span><span> We aimed to evaluate the possible links among REM sleep duration, continuous glucose levels, and gut microbiota composition.</span></p> <p><strong><span>Design</span></strong><span>: This is an observational, prospective, real-life, cross-sectional case-control study. </span></p> <p><span><strong>Setting</strong>: </span><span>Tertiary Hospital recruiting healthy volunteers.</span></p> <p><span><strong>Patients or Other Participants</strong>:</span><span> One-hundred and eighteen (60 with obesity), middle-aged (39.1-54.8) subjects.</span></p> <p><span><strong>Intervention(s)</strong>:</span><span> Glucose variability and REM sleep duration were assessed by 10-day continuous glucose monitoring (CGM) (Dexcom G6®) and wrist-actigraphy (Fitbit Charge 3®), respectively</span></p> <p><span><strong>Main Outcome Measure(s)</strong>:</span><span>. Glucose variability was evaluated through standard deviation (SD), coefficient of variation (CV), and interquartile range (IQR). The percentage of time in range (% TIR), 126-139 mg/dL (TIR2), and 140-199 mg/dL (TIR3) were calculated. Shotgun metagenomics sequencing was applied to study gut microbiota taxonomy and functionality. </span></p> <p><span><strong>Results</strong>:</span><span> Increased glycemic variability (SD, CV, and IQR) was observed among subjects with obesity in parallel to increased % TIR2 and % TIR3. REM sleep duration was independently associated with the % TIR3 (β=-0.339; p<0.001) and glucose variability (SD, β=-0.350; p<0.001). Microbial taxa from Christensenellaceae family (Firmicutes phylum) were positively associated with REM sleep and negatively with glucose continuous monitoring levels, while bacteria from Enterobacteriacea family and bacterial functions involved in iron metabolism showed opposite associations. </span></p> <p><span><strong>Conclusions</strong>:</span><span> Decreased REM sleep duration was independently associated with a worse glucose profile. The associations of species from Christensenellaceae and Enterobacteriaceae families with REM sleep duration and continuous glucose values suggest an integrated picture of metabolic health.</span></p>
Gene expression data from clones of FAO cells with different glucose production capability
<div> <div> <div> <p>In response to energy and nutrient shortage, the liver triggers several catabolic processes to promote survival. Despite recent progresses, the precise molecular mechanisms regulating the hepatic adaptation to fasting remain incompletely characterized. Here, we report the identification of Hydroxysteroid dehydrogenase-like 2 (HSDL2) as a mitochondrial protein highly induced by fasting. We show that activation of PGC1a-PPARa and inhibition of the PI3K- mTORC1 axis stimulate HSDL2 expression in hepatocytes. We found that HSDL2 depletion decreases cholesterol conversion to bile acids (BAs) and impairs FXR activity. HSDL2 knockdown also reduces mitochondrial respiration, fatty acid oxidation, and TCA cycle activity. Bioinformatics analyses revealed that hepatic Hsdl2 expression positively associates with the postprandial excursion of various BA species in mice. Here, we show that liver-specific HSDL2 depletion impacts BA metabolism and decreases circulating cholesterol levels upon refeeding. Overall, our report identifies HSDL2 as a fasting-induced mitochondrial protein that links nutritional signals to BAs and cholesterol homeostasis.</p> </div> </div> </div>
19307_2020_10_22_downUpshift_2_01_2_glucose_dual_pH__dot6_nrg1_tod6__00 (part 1)
High throughput time lapse experiment. Details can be found on the 'txt' files inside.
Brown adipose tissue PET-MR after fructose and glucose intervention
<p>Includes the data and MATLAB functions used to produce the manuscript: "High-fructose feeding suppresses cold-stimulated brown adipose tissue glucose uptake in young men independently of changes in thermogenesis and the gut microbiome"</p>
Large excess capacity of glycolytic enzymes in Saccharomyces cerevisiae under glucose-limited conditions
<p>Computational models and figure data for the publication "Large excess capacity of glycolytic enzymes in <em>Saccharomyces cerevisiae </em>under glucose-limited conditions" (to be submitted). Data put together by Pranas Grigaitis, p.grigaitis [at] vu.nl.</p> <p> </p> <p><em>Abstract</em></p> <p>In Nature, microbes live in very nutrient-dynamic environments. Rapid scavenging and consumption of newly introduced nutrients therefore offer a way to outcompete competitors. This may explain the observation that many microorganisms, including the budding yeast <em>Saccharomyces cerevisiae,</em> appear to keep “excess” glycolytic proteins at low growth rates, i.e. the maximal capacity of glycolytic enzymes (largely) exceeds the actual flux through the enzymes. However, such a strategy requires investment into preparatory protein expression that may come at the cost of current fitness. Moreover, at low nutrient levels, enzymes cannot operate at high saturation, and overcapacity is poorly defined without taking enzyme kinetics into account.</p> <p>Here we use computational modeling to suggest that in yeast the overcapacity of the glycolytic enzymes at low specific growth rates is a genuine excess, rather than the optimal enzyme demand dictated by enzyme kinetics. We found that the observed expression of the glycolytic enzymes did match the predicted optimal expression when <em>S. cerevisiae</em> exhibits mixed respiro-fermentative growth, while the expression of tricarboxylic acid cycle enzymes always follows the demand. Moreover, we compared the predicted metabolite concentrations with the experimental measurements and found the best agreement in glucose-excess conditions. We argue that the excess capacity of glycolytic proteins in glucose-scarce conditions is an adaptation of <em>S. cerevisiae</em> to fluctuations of nutrient availability in the environment.</p>
Gastric Residual Volume, Safety and Effectiveness of Drinking 250ml Glucose Solution 2-3 Hours before Surgery in Gastric Cancer Patients: A Multicenter, Single-blind, Randomized Controlled Trial
<p><strong>Supplementary Figure 1</strong></p> <p> </p> <p>A. Change of QUICKI level after surgery</p> <p>Post-OP: right after operation; POD: post-operation day; Mixed linear model statistics showed that the effect of time ( p=0.004) was significant, but no significant differences were noted for group(P=0.600) or group*time(P=0.963).</p> <p>B. Change of Recovery Level of QUICKI after surgery</p> <p>Post-OP: right after operation; POD: post-operation day; Mixed linear model statistics showed that no significant differences were noted for group(P=0.600) ,time (P=0.235) or group×time(P=0.963).</p> <p>C. Change of WBC level after surgery</p> <p>Post-OP: right after operation; POD: post-operation day; Mixed linear model statistics showed that the effect of time ( p<0.001) was significant, and no significant differences were noted for group(P=0.392) or group×time(P=0.314).</p> <p>D. Change of CRP level after surgery</p> <p>Post-OP: right after operation; POD: post-operation day; Mixed linear model statistics showed that the effect of time ( p<0.001) was significant, but no significant differences were noted for group(P=0.312) or group × time(P=0.826).</p>
Photoreceptor glucose metabolism determines normal retinal vascular growth
<p>The neural cells and factors determining normal vascular growth are not well defined even though vision-threatening neovessel growth, a major cause of blindness in retinopathy of prematurity (ROP) (and diabetic retinopathy), is driven by delayed normal vascular growth. We examined if hyperglycemia and low adiponectin (APN) levels delayed normal retinal vascularization, driven primarily by dysregulated photoreceptor metabolism.</p> <p>One part of the experiments was to use targeted quantitative proteomics to measure the expression of proteins with selected reaction monitoring. We measured the enzymes in glycolysis, the Krebs cycle, and several addition mitochondrial proteins.</p> <p>We found that in a neonatal mouse model of postnatal hyperglycemia modeling early ROP, hyperglycemia caused photoreceptor dysfunction and delayed neurovascular maturation associated with changes in the APN pathway; recombinant mouse APN or APN receptor agonist adipoRon treatment normalized vascular growth. APN deficiency decreased retinal mitochondrial metabolic enzyme levels particularly in photoreceptors, suppressed retinal vascular development and decreased photoreceptor platelet-derived growth factor (Pdgfb). APN pathway activation reversed these effects. Blockade of mitochondrial respiration abolished adipoRon-induced Pdgfb increase in photoreceptors. Photoreceptor-knockdown of Pdgfb delayed retinal vascular formation. Stimulation of the APN pathway might prevent hyperglycemia-associated retinal abnormalities andsuppress Phase I ROP in premature infants.</p>
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