mM Of Glucose Research Articles

Anticataract Activity of Ethanolic Extract of Garcinia Mangostana Linn Pericarp on Glucose-induced Cataractogenesis in Goat Lens

BACKGROUND: One of the main causes of blindness for diabetic patients is cataract. The molecular mechanisms that may be involved in diabetic cataract include polyol pathway flux, increased formation of advanced glycation end products, osmotic stress, and elevated oxidative stress.
 AIM: The aim of the study was to explore the anticataract activity of the ethanol extract from pericarp of Garcinia mangostana Linn (GML) in Goat eye lens.
 METHODS: Goat eye lenses separated to five groups were incubated in M199 medium, added by penicillin of 100 U/ml and streptomycin of 0.1 mg/ml in a 37°C incubator with 95% O2 and 5% CO2 for 120 h. Group I served as the normal control. Group II (toxic control) the lenses were added by 30 mM glucose. The lenses in Groups III, IV, and V nurtured in M199 medium with 30 mM of glucose added by 100, 500, and 1000 μg/ml of GML pericarp extract. Carboxymethyllysine (CML), GRP78, DDIT3, active caspase 3, and MDA levels were measured by enzyme-linked immunosorbent assay assays. Comparisons of biochemical parameters were conducted using one-way ANOVA with post hoc Tukey test.
 RESULTS: The administration of glucose 30 mM increased MDA, CML, DDIT3, and GRP78, and active caspase 3 levels in Group II. Groups III, IV, and V which treated with GML pericarp extract decreased MDA, CML, GRP78, and DDIT3, and active caspase 3 levels inside the lens. On lens capsule, the CML and GRP78 levels increased.
 CONCLUSION: Ethanol extract of GML pericarp potentially showed antioxidant, anti-glycation, DDIT3 inhibitor, and anti-apoptotic activity in Goat cultured lenses.

Glucose Loading Enhances the Value of 18F-FDG PET/CT for the Characterization and Delineation of Cerebral Gliomas.

This study aimed to assess how to enhance the value of 18F-Fluorodeoxyglucose (FDG) PET/CTs for glioma grading and better delineation of the tumor boundary by glucose loading. In mouse models of brain tumor using U87MG cells, 18F-FDG-PET images were obtained after fasting and after glucose loading. There was a significant difference in the tumor-to-normal cortex-uptake ratio (TNR) between the fasting and glucose-loading scans. 14C-2-Deoxy-D-glucose (14C-DG) uptake was measured in vitro using U87MG, U373MG and primary neurons cultured with different concentrations of glucose. The tumor-to-neuron ratio of 14C-DG uptake increased with up to 10 mM of glucose. Finally, 10 low-grade and 17 high-grade glioma patients underwent fasting and glucose loading 18F-FDG PET/CT and the TNR was compared between scans. The effect of glucose loading was significant in high-grade but not in low-grade gliomas. The receiver operating characteristic curve analyses with a cut-off TNR of 0.81 showed a higher area under the curve after glucose loading than fasting for differentiating low-grade versus high-grade gliomas. In addition, the glucose loading PET/CT was more useful than the fasting PET/CT for the discrimination of oligodendrogliomas from IDH-wildtype glioblastomas. Glucose loading resulted in a greater reduction in 18F-FDG uptake in the normal cortex than in tumors, which increases the usefulness of 18F-FDG PET/CT for grading.

Glucose-Induced Expression of DAPIT in Pancreatic β-Cells

Transcript levels for selected ATP synthase membrane FO-subunits—including DAPIT—in INS-1E cells were found to be sensitive to lowering glucose down from 11 mM, in which these cells are routinely cultured. Depending on conditions, the diminished mRNA levels recovered when glucose was restored to 11 mM; or were elevated during further 120 min incubations with 20-mM glucose. Asking whether DAPIT expression may be elevated by hyperglycemia in vivo, we studied mice with hyaluronic acid implants delivering glucose for up to 14 days. Such continuous two-week glucose stimulations in mice increased DAPIT mRNA by >5-fold in isolated pancreatic islets (ATP synthase F1α mRNA by 1.5-fold). In INS-1E cells, the glucose-induced ATP increment vanished with DAPIT silencing (6% of ATP rise), likewise a portion of the mtDNA-copy number increment. With 20 and 11-mM glucose the phosphorylating/non-phosphorylating respiration rate ratio diminished to ~70% and 96%, respectively, upon DAPIT silencing, whereas net GSIS rates accounted for 80% and 90% in USMG5/DAPIT-deficient cells. Consequently, the sufficient DAPIT expression and complete ATP synthase assembly is required for maximum ATP synthesis and mitochondrial biogenesis, but not for insulin secretion as such. Elevated DAPIT expression at high glucose further increases the ATP synthesis efficiency.

Power generation and autonomous glucose detection with an integrated array of abiotic fuel cells on a printed circuit board

Wearable technologies can enable effective management of life-threatening diseases. In such systems, miniaturisation leads to minimally invasive and lightweight devices that, whilst ensuring safety, allow patients to perform their everyday activities freely. By generating direct and continuous energy from physiological fluids at body temperature, glucose fuel cells (GFCs) provide an attractive and easy-to-miniaturise power source alternative to lithium batteries. In this context, we explore for the first time the use of printed circuit boards (PCBs) for the development of integrated arrays of abiotic GFCs and successfully demonstrate their operation at physiological concentrations of glucose, both in a phosphate buffer and in synthetic interstitial fluid. Each GFC consists of a porous gold anode and a Pt/Au cathode in a single layer, and generates a maximum power of 14.3 μW cm−2 (in 6 mM of glucose), with a linear response to glucose within a concentration range that includes hypo- and hyper-glycaemic values. We also demonstrate linear power output scale-up by electrically connecting in parallel four GFCs on PCB. Considering the simplicity of the system architecture and the ease of integration provided by PCBs, our pioneering work paves the way for exciting opportunities in the field of self-powered wearable diagnostics.

Purification and characterization of glucoamylase of Aspergillus oryzae from Luzhou-flavour Daqu.

To obtain novel glucoamylase from Daqu microbe. A dominant strain known as LZ2 with high activity of hydrolyzing starch was isolated from Luzhou Daqu, a Chinese traditional fermentation starter. The LZ2 was identified as Aspergillus oryzae by 18S rDNA sequence analysis. Glucoamylase from LZ2, named as GA-LZ2, was purified to homogeneity and showed a single band with expected molecular mass of 60 kD. The GA-LZ2 effectively degraded amylose, rice starch and wheat starch. Optimal temperature and pH value of enzyme were 60 °C and pH 4.0 respectively. The GA-LZ2 displayed significant thermal stability and pH stability at moderate temperature and low pH. Intriguingly, the thermostability was enhanced in the presence of starch. In addition, GA-LZ2 exhibited insensitivity to glucose, independence of metal ions and tolerance to organic solvents. The GA-LZ2 retained complete activity in the presence of 100mM glucose and 5% ethanol and methanol. Glucoamylase GA-LZ2 displayed broad substrate specificity, strong stability and tolerance, suggesting that GA-LZ2 carry potential for industrial application in bioethanol production.

A Novel Glucose-Tolerant GH1 β-Glucosidase and Improvement of Its Glucose Tolerance Using Site-Directed Mutation.

A novel GH1 β-glucosidase gene (bgla) from marine bacterium was sequenced and expressed in Escherichia coli. After purification by Ni2+ affinity chromatography, the recombinant protein was characterized. The purified recombinant enzyme showed maximum activity at 40°C, pH7.5 and was stable between temperatures that range from 4 to 30°C and over the pH range of 6-10. The enzyme displayed a high tolerance to glucose and maximum stimulation at the presence of 100mM glucose. To improve glucose tolerance of the enzyme, a site-directed mutation (f171w) was introduced into β-glucosidase. The recombinant F171W showed a higher glucose tolerance than the wild type and maintained more than 40% residual activity at the presence of 4M glucose. Additionally, the recombinant enzymes showed notable tolerance to ethanol. These properties suggest the enzymes may have potential applications for the fermentation of lignocellulosic sugars and the production of biofuels.

Cotton thread-based wearable sensor for non-invasive simultaneous diagnosis of diabetes and kidney failure

Thread has become a promising substrate for non-invasive wearable sensor. Herein, we create a modified cotton thread-based colorimetric sensor for non-invasive and simultaneous detection of glucose and urea excreted from human sweat. Cellulose nanofiber/chitosan-graphene oxide was selected to modify the cotton thread surfaces for enhancing of enzymatic immobilization efficiency and sensor performance. The modified thread surfaces were characterized by scanning electron microscopy and X-ray photoelectron spectroscopy. This sensing platform exhibits a linear range of 0.1–3 mM with a detection limit of 0.1 mM for glucose and a linear range of 30–180 mM with a detection limit of 30 mM for urea. Interestingly, this colorimetric sensor can determine the cut-off levels for both glucose (0.3 mM) and urea (65 mM) in human sweat, thus it can effectively distinguish between normal and abnormal people. Due to the thread flexibility nature, this sensor can be readily integrated with the clothes and accessories for real-time and continuous monitoring of diabetes and kidney failure from the wearer’s sweat. This platform might open a new road for blood-free diagnosis in healthcare applications.

Oxidation of energy substrates in tissues of largemouth bass (Micropterus salmoides).

This study tested the hypothesis that amino acids are oxidized at higher rates than glucose and palmitate for ATP production in tissues of largemouth bass (LMB, a carnivorous fish). Slices (10 to 50 mg) of liver, proximal intestine, kidney, and skeletal muscle isolated from LMB were incubated at 26°C for 2h in oxygenated Krebs-Henseleit bicarbonate buffer (pH 7.4, with 5mM D-glucose) containing either D-[U-14C]glucose, 2mM L-alanine plus L-[U-14C]alanine, 2mM L-aspartate plus L-[U-14C]aspartate, 2mM L-glutamate plus L-[U-14C]glutamate, 2mM L-glutamine plus L-[U-14C]glutamine, 2mM L-leucine plus L-[U-14C]leucine, or 2mM palmitate plus [U-14C]palmitate. In parallel experiments, tissues were incubated with a [U-14C]-labeled tracer and a mixture of unlabeled substrates [alanine, aspartate, glutamate, glutamine, leucine, and palmitate (2mM each) plus 5mM glucose]. 14CO2 was collected to calculate the rates of substrate oxidation. In separate experiments, O2 consumption by each tissue was measured in the presence of individual or a mixture of substrates. The activities of key metabolic enzymes were also measured. Results indicated that the liver and skeletal muscle had a limited ability to oxidize glucose and palmitate to CO2 for ATP production in the presence of individual or a mixture of substrates due to low activities of carnitine palmitoyltransferase-I, hexokinase and pyruvate dehydrogenase. In the presence of individual substrates, each amino acid was actively oxidized by all the tissues. In the presence of a mixture of substrates, glutamine and glutamate were the major metabolic fuels in the proximal intestine and kidney, as glutamine for the liver and aspartate for skeletal muscle. All the tissues had high activities of glutaminase, glutamate dehydrogenase, and transaminases. At the same extracellular concentration of amino acids (2 mM) in a mixture of energy substrates, glutamine was the major metabolic fuel for the liver of the LMB, glutamine and glutamate for the proximal intestine and kidneys, and aspartate for the skeletal muscle. Glutamine plus glutamate plus aspartate generated 60-70% of ATP in LMB tissues.

THE EFFECT OF 5 µM DOSAGE OF AMLODIPINE ON NRF2 EXPRESSION IN NEURON CULTURE INDUCED BY 25 mM OF GLUCOSE

Introduction: Hyperglycemia on neuron cell culture occurs when the cells are induced by 25 mM of glucose. Hyperglycemia state will increase intracellular Ca2+ that leads to increased of oxidative stress in the cell. This causes the activation of antioxidant enzymes by Nrf2 protein. Amlodipine act on nerve cells through bounding with L-Type Calcium Channel (LTCC). 5 µM of amlodipine has neuroprotective effect on cell culture of neuron by inhibiting cell death. Aim: The purpose of this research is to know the effect of treating amlodipine dose 5 μM towards expression of the protein Nrf2 in SH-SY5Y cell culture induced by 25 mM glucose. Methods: In this research on neuron cell culture induced 25 mM glucose within 6 days and treated with amlodipine and without amlodipine 5 µM. Results: Based on research results obtained test results independent t test (p = 0,324) that there is no change of the Nrf2 expression significant between a given neuron cell culture with amlodipine without amlodipine. Spearman correlation test showed (r = 0.290; p = 0.361) that treating by amlodipine 5 µM not significantly increasing Nrf2 expression. Conclusion: Based on this study it can be concluded that treating by amlodipine 5 µM not give effect against Nrf2 expression on neuron cell culture induced 25 mM glucose.

P0967ENHANCING PODOCYTE REGENERATION WITH BROMOINDIRUBIN-3´-OXIME (BIO) AS A POTENTIAL TERAPEUTIC TARGET IN DIABETIC KIDNEY DISEASE

Abstract Background and Aims Diabetic nephropathy (DN) is a leading cause of end-stage kidney disease. RAS and SGLT2 inhibitors are well established in reducing the progression of DN in early stages but true tissue regeneration is not achieved. BIO, a glucose synthase kinase 3 inhibitor (GSK3β), improves outcomes in non-diabetic kidney injury by enhancing podocyte regeneration from local podocyte progenitors. We hypothesized that treating podocytes in hyperglycemic conditions with BIO could revert the oxidative stress damage typically seen in DN. Method To study the effect of BIO on podocytes, we isolated glomeruli from wildtype mice by perfusing them with magnetic beads and stimulated the purified glomeruli for 24 hours with or without 10µM BIO in presence or absence of 30mM glucose. The response to the stimuli was assessed by characterizing the overall gene expression via RT-qPCR. Additionally, differentiated murine podocytes (K5P5) and murine glomerular endothelial cells (GEnCs) were stimulated under the same conditions with the same subsequent readouts to differentiate the response of podocytes from that of the endothelial compartment. To understand, if BIO could represent a potential new therapeutic option under the aspect of pharmacological safety, we uninephrectomized male BKS-Lepr-/- mice, fed them with a salt-free chow to induce DN. To mimic the human condition more closely we treated the mice with and without BIO, but in presence of the human standard of care therapy (SOC; metformin, ramipril, empagliflozin), which could potentially identify adverse pharmacological interactions. After 16 weeks kidney, heart, pancreas, sciatic nerve, liver, blood, skeletal muscle and adipose tissue were collected for histopathological and gene expression analysis. Results While glucose exposure induced a strong reduction of nephrin gene expression in whole glomeruli, BIO reverted the effect, indicating a protective effect on podocytes (30 mM glucose: 0.447, ci 0.224 – 0.724; 30 mM glucose+BIO: 1.837, ci 1.205 – 2.505, p-value=0.029, Fig.A). Similar results were found in differentiated murine podocytes, in which BIO treatment significantly increased podocin gene expression after 7 days of culture (0.920, ci 0.820 – 1.34, 3.561 ci 1.756 – 7.909, p-value=0.029), also here suggesting a protective effect of BIO on glucose-induced podocyte (Fig.B). In contrast, BIO showed no effect on endothelial cell-specific markers in murine GEnCs, indicating a podocyte-specific effect of BIO. A comparable effect of BIO on podocytes was observed in vivo, as well. Diabetic mice treated with SOC and BIO showed borderline increased renal podocin gene expression levels (2.177 ci 0.830 – 2.739) compared to SOC alone (1.188 ci 0.378 – 2.194 ,p-value = 0.064), but did not modify markers of inflammation, such as IL-6, or fibrosis, such as fibronectin (Fig.C). The extended safety analysis of non-renal organs did not reveal any safety concern of the SOC/BIO combination in comparison to SOC alone in any of the analyzed tissues. Conclusion The current study revealed that BIO has protective effects on podocytes in vitro and might as well have renoprotective effects in DN in vivo by enhancing podocyte regeneration without showing any safety-related issues.

An ultrasimple and cost‐effective µPAD by pasting hydrophilic channels to a hydrophobic basement

AbstractThe application of the paper‐based microfluidic device (µPAD) as a potentially significant platform for clinical diagnoses has gained a great interest during the recent years. This work presented a technically ultrasimple, low‐cost, effective, and rapid method for the µPADs fabrication by pasting a hydrophilic flower‐like paper mask to a hydrophobic PVC substrate, which was purchased with adhesive on it. The whole manufacture process could be implemented in a few seconds by untrained personnel. To demonstrate the feasibility of this method in real‐world situations, the developed paper device was employed for colorimetric assays of glucose in artificial urine and nitrite in artificial saliva. The main analysis parameters, for example, the optimum volumes of reagents, reaction time, and so forth, were seriatim optimized. Under optimal conditions, the detection limits were 0.9 mM and 19.5 µM for glucose and nitrite, respectively; the detection ranges were 0.9–30 mmol/L and 19.5–312.5 µmol/L for glucose and nitrite analyses, respectively. These results showed that this equipment‐free µPAD had great potentials for the qualitative or semiquantitative detection of glucose and nitrite in real samples.

451-P: Proteome Profiling in Rat Cardiomyoblasts: Understanding Diabetic Cardiomyopathy

Introduction: Diabetic cardiomyopathy is characterized by oversupply of nutrients with concurrent loss of metabolic flexibility. Even in excess substrate availability the heart suffers energy depletion as metabolic fluxes are diminished. We established a stably GLUT4 overexpressing cell line derived from H9C2 that presents a diabetic cardiomyopathy like phenotype. Protein expression patterns are analyzed by proteomic approaches. Material and Methods: Rat cardiomyoblasts stably overexpressing GLUT4 (H9C2-GLUT4) were cultured under hyperglycemic conditions (30mM glucose) either short time (3 days) or long time (more than 3 months). Expression profile was compared to non-transfected H9C2 cells (H9C2), using same culture conditions. Cell culture samples were prepared for mass spectrometric analysis by sample lysis followed by tryptic digestion. Peptides were analyzed on an Orbitrap Elite (ThermoFisher, Scientific) and resulting files were taken for the identification and quantification of proteins using MaxQuant and Perseus. DAVID Bioinformatics Resources 6.8 functioned as Pathway and GO term enrichment tool for further in depth analysis of the data set. Results: We were able to quantify 2,841 proteins of whose 881 were found to be significantly regulated (5% FDR; ANOVA corrected p-value). Further analysis of long time and short time exposure of either WT or GLUT4 overexpressing cells lead to the identification of 135 significantly expressed proteins in the WT and 112 significantly expressed proteins in the H9C2-GLUT4 model (5% FDR; ANOVA corrected p-value). In depth pathway and GO term enrichment analysis support effects on metabolism, protein biosynthesis and handling, and ECM composition. Discussion: Chronic glucose overload in cardiomyoblasts induced by GLUT4 overexpression and hyperglycemia resulted in a metabolic induced proteome profile change. These models may thus increase our knowledge of biological effects of chronic hyperglycemia on the diabetic heart. Disclosure B. Stratmann: Speaker’s Bureau; Self; AstraZeneca, Neoplas Tools GmbH. B. Eggers: None. Y. Mattern: None. K. Marcus: None. D. Tschoepe: Advisory Panel; Self; AstraZeneca, Boehringer Ingelheim International GmbH. Research Support; Self; AstraZeneca, Bayer AG, Boehringer Ingelheim International GmbH, Neoplas tools GmbH.

574-P: Antioxidant Defence and Long Noncoding RNA in Diabetic Retinopathy

Retinal oxidative stress is increased and the antioxidant defence system is compromised in diabetic retinopathy. Expression of many key antioxidant genes is regulated by a master regulator, nuclear factor erythroid 2-related factor (Nrf2). The transcriptional activity of Nrf2 is mediated by an intracellular inhibitor Kelch-like ECH-associated protein 1 (Keap1), which regulates its nuclear movement. In diabetes, Nrf2 transcriptional activity is decreased and Keap1 levels are increased. A long noncoding RNA (IncRNA), Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1), plays a role in regulating Keap1 expression, and retinal MALAT1 levels are upregulated in diabetes. Our aim is to investigate the role of MALAT1 in maintaining the antioxidant defence system in diabetic retinopathy. Human retinal endothelial cells (untransfected or transfected with MALAT1-siRNA) were incubated in 20mM glucose for 96 hours. MALAT1 expression was analysed by q-RTPCR and RNA sequencing, and role of MALAT1 in Keap1 transcription was quantified using MALAT1 RNA pull down assay. Simultaneous occupancy of MALAT1 and transcription factor Sp1 on Keap1 promoter was quantified by Chromatin Isolation by RNA Purification (ChIRP)-reChIP technique, nuclear translocation of Nrf2 by immunofluorescence imaging, and Nrf2-responsive genes superoxide dismutase 2 (Sod2) and heme oxygenase 1 (HO1) by q-RTPCR. Compared to cells in 5mM glucose, high glucose increased co-occupancy of MALAT1 and Sp1 at Keap1 promoter. MALAT1-siRNA ameliorated glucose-induced increase in co-occupancy of MALAT1-Sp1 at its promoter and decreased Keap1 expression. MALAT1-siRNA also restored nuclear localization of Nrf2 and the transcription of Sod2 and HO1. Thus, IncRNA MALAT1, via Keap1, modulates the transcriptional activity of Nrf2 and the antioxidant defence system in diabetic retinopathy. Regulation of MALAT1 can protect the retina from oxidative damage, and prevent/slow down the development of diabetic retinopathy. Disclosure R. Kowluru: None. R. Radhakrishnan: None. Funding EY014370, EY017313, EY022230

455-P: Pan-ErbB Inhibition Attenuates Diabetes-Induced Vascular Dysfunction in an Experimental Model of Diabetes

The underlying mechanisms leading to diabetes-induced vascular complications are not fully understood. We have previously shown that epidermal growth factor receptor (EGFR), which is part of the four membered family of EGFR/ErbB receptor tyrosine kinases, appears to play a detrimental role. However, the role of the other ErbB family members (ErbB2, ErbB3, and ErbB4)- that regulate cell growth, proliferation, differentiation and apoptosis- is not fully known and was further evaluated in this study. In a streptozotocin-rat model of type 1 diabetes, 4-weeks of diabetes induced significant vascular dysfunction, as assessed by abnormally high vasoconstrictor responses to norepinephrine in the mesenteric vascular bed (MVB). Diabetes also led to increased phosphorylation of all ErbB receptors with subsequent increased phosphorylation of downstream ERK1/2 in the MVB. Chronic 4-week in vivo administration of a novel pan-ErbB inhibitor, generation 7 polyamidoamine dendrimer (G7PAMAM; 20mg/kg daily i.p), or the well-established pan-ErbB inhibitor, Genistein (1mg/kg i.p. alt diem) to diabetic rats led to a marked attenuation in the hyperphosphorylation of all ErbBs, ERK1/2 and to a significant correction in NE-mediated hyper-responsiveness of the diabetic MVB. Furthermore, pan-ErbB inhibitors attenuated high glucose-induced ErbBs-ERK1/2 signaling in primary vascular smooth muscle cells grown in high (25mM) glucose. These data show for the first time that pan-ErbB inhibition attenuates diabetes-induced vascular dysfunction in an experimental model of diabetes. Therefore, pan-ErbB inhibition might represent a novel strategy for the treatment of diabetes-induced vascular complications. Disclosure S. Akhtar: None. B. Chandrasekhar: None. I. Benter: None. Funding Qatar University (QUCG-CMED-19/20-3)

Enhancement anti-interference ability of photoelectrochemical sensor via differential molecularly imprinting technique demonstrated by dopamine determination

Molecularly imprinting polymers (MIPs), as artificial antibodies with high recognition selectivity to template molecules, are widely used in various biosensors. To improve further the selectivity of MIPs-based photoelectrochemical (PEC) biosensors, we report a differential strategy using non-imprinted polymers (NIPs) as the reference. In a proof-to-concept example for the determination of dopamine (DA), MIPs and NIPs membranes were fabricated by electrochemical polymerization of polypyrrole membranes on the surface of graphene quantum dots (GQDs)/TiO2 nanotubes (NTs). The photocurrent difference between the two PEC cells, MIPs@GQDs/TiO2 NTs−Pt and NIPs@GQDs/TiO2 NTs−Pt, was measured as the signal. As the non-specific adsorption of non-template molecules on the outside surface of MIPs and NIPs membranes is similar, the anti-interference ability for the determination of DA is much improved by using differential strategy. In the normal and differential PEC measurement models, 10.0 μM ascorbic acid is equivalent to 3.12 and 0.40 μM DA, respectively. Further, the smaller specific surface area in NIPs membrane was compensated by using a weight factor to correct the residual interference in a modified differential model. By using 10.0 μM ascorbic acid as the balance point, the presence of 10.0 μM H2O2, glutathione, uric acid or glucose is equivalent only to 0.090, 0.061,0.11 or 0.041 μM of DA, respectively, which are about 3–7% of their interference levels in the normal photocurrent model. The differential PEC method was applied in the determination of DA in serum samples in the linear range of 0.05–12.5 μM, with the detection limit of 0.018 μM.

Using G‐Rich Sequence to Enhance the Peroxidase‐Mimicking Activity of DNA‐Cu/Ag Nanoclusters for Rapid Colorimetric Detection of Hydrogen Peroxide and Glucose

AbstractFour kinds of DNA‐based Ag and Cu/Ag nanoclusters (NCs) were synthesized and their fluorescence properties were investigated at pH 7.0 and 5.5. Among them the Cu/Ag NCs templated by DNA containing both C‐rich and G‐rich sequences (the c‐myc TBA−Cu/Ag NCs) give the strongest and the most stable fluorescence emission at ∼555 nm under neutral and acidic conditions. Unexpectedly, the c‐myc TBA−Cu/Ag NCs can catalyze efficiently and rapidly the reaction of hydrogen peroxide (H2O2) with 3,3′,5,5′‐tetramethylbenzidine (TMB) to produce blue TMB oxide (TMBox) under acidic conditions, indicating the high peroxidase‐mimicking activity. Based on this nanozyme the detection for H2O2 and glucose was performed using colorimetric method. The results indicate that the linear range of detection for H2O2 is from 0.1 to 1 mM with the detection limit (LOD) of 7.42 μM, while the linear range is from 0.1 to 0.7 mM and LOD was calculated to be 9.38 μM for glucose. Additionally, glucose can be successfully detected in diluted serum samples and has an acceptable recovery rate, indicating that this nanozyme has a potential application prospect.

MiR-7 Reduces High Glucose Induced-damage Via HoxB3 and PI3K/AKT/mTOR Signaling Pathways in Retinal Pigment Epithelial Cells.

Diabetic retinopathy (DR) is a common complication of diabetes. This study investigated the effect of miR-7 in the regulation of cell proliferation via the HoxB3 gene and PI3K/AKT/mTOR signaling pathways in DR. Human retinal pigment epithelial cell line (ARPE-19) cultured in normal medium (Control) and high glucose medium (25mM glucose, HG) was transfected with mimics NC (HG+ mimics NC), miR-7 mimics (HG+miR-7 mimics), inhibitor NC (HG+ inhibitor NC), and miR-inhibitor (HG+miR-7 inhibitor). The cells were assayed for viability, apoptosis, and expression of genes. HG reduced cell viability and increased apoptosis. However, miR-7 mimics reduced the apoptosis. PCR results showed that miR-7 was significantly upregulated after transfection with miR-7 mimics. The expression of Hoxb3, mTOR, p-PI3K, and p- AKT was significantly downregulated at mRNA and protein levels after miR-7 mimics transfection, while no difference was observed for PI3K and AKT expression. Our findings demonstrate that miR-7 regulates the growth of retinal epithelial cells through various pathways and is a potential therapeutic target for the prevention and treatment of diabetic retinopathy.

Lectin Affinity Based Recognition Nanomaterial for Glucose

Glucose is an important biomolecule because it is an important source of energy for cells and is used as an intermediate/metabolic agent. Selective recognition of glucose is important for diagnosing many metabolic diseases. In this study, lectin ligand (Con A) attached p(GMA) nanopolymer was synthesized and characterized. The best interaction of p(GMA)-ConA nanopolymer and glucose was determined to be 10mM glucose concentration at pH = 8.0. In the selectivity assay, p(GMA)-Con A was found to be 2-fold selective for glucose than galactose. Lectin affinity based nanopolymeric system that is selective, with high surface area, low cost and highly biocompatible with high adsorption capacity has been developed for recognition of glucose.

Ni3S2 Supported on Porous Ball‐milled Silicon, a Highly Selective Electrochemical Sensor for Glucose Determination

AbstractIn this work, an electrochemical sensor based on Ni3S2 nanoparticles supported on porous ball‐milled silicon was fabricated for measuring glucose. At first, the glassy carbon electrode (GCE) surface was modified by Ni3S2 nanoparticles supported on a porous ball‐milled silicon substrate. To characterize the modified electrode, N2 adsorption‐desorption isotherms and BHJ, transmission electron microscopy (TEM), scanning electron microscopy (SEM), energy‐dispersive X‐ray spectroscopy (EDX), elemental mapping and X‐ray diffraction (XRD) were used. In the following, the effective parameters on the sensor response such as pH, NaOH concentration, catalyst concentration, applied potential, and rotational speed of the electrode were optimized using cyclic voltammetric (CV) and hydrodynamic amperometric methods. Under the optimal conditions, the calibration curve was plotted using the hydrodynamic amperometric method. Three linear regions were obtained from 0.5–134, 134–1246, and 1246–3546 μM, with a detection limit of 0.2 μM for glucose. Finally, the proposed method was used for measuring glucose levels in human blood serums.

Lamellar FeOcPc‐Ni/GO Composite‐Based Enzymeless Glucose Sensor

AbstractDiabetes is a serious yet controllable disease, primarily caused by a disorder in insulin production, which has become a major public health problem worldwide, motivating the development of enzymatic and non‐enzymatic electrochemical glucose sensors. In this work, a lamellar composite was prepared by coordinating nickel(II) ions on graphene oxide (GO) sheets and then attaching iron octacarboxyphthalocyanine (FeOcPc) and nickel hydroxide (Ni) on the nickel sites leading to their stacking and formation of a stable material for enzymeless glucose sensor, through a facile solvothermal route. The new composite was shown to be formed by amorphous and ultrasmall α‐Ni(OH)2 nanoparticles that are not easily converted to the less active β‐Ni(OH)2 phase even in the presence of 5 mM of glucose, asserting its stability and reproducibility, allied to a sensitivity as high as 192.13 μA mM−1 cm−2, and a limit of detection as low as 0.625 μM.