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Printing techniques hold great potential in the manufacture of electronics such as sensors, micro-supercapacitors, and flexible electronics. However, developing large-scale functional conductive inks with appropriate rheological properties and active components still remains a challenge. Herein, through optimizing the formulations of ink, iron single sites supported N-doped carbon black (Fe1-NC) inks can serve as both conductive electrodes and high-reactive catalysts to realize convenient glucose detection, which pronouncedly reduces the dosage of enzyme and simplifies the sensors preparation. In detail, utilizing in-situ pyrolysis method, Fe1-NC single-atom catalysts (SACs) are prepared in bulk (dekagram-level). The batched Fe1-NC SACs materials can be uniformly mixed with modulated ink to realize the screen printing with high resolution and uniformity. Also, the whole scalable preparation and ink-functional process can be extended to various metals (including Co, Ni, Cu, and Mn). The introduction of highly active Fe1-NC sites reduces the amount of enzyme used in glucose detection by at least 50%, contributing to the cost reduction of sensors. The strategy in harnessing the SACs onto the carbon inks thus provides a broad prospect for the low-cost and large-scale printing of sensitive sensing devices. [ABSTRACT FROM AUTHOR]

Glucose mainly serves as an energy source, highly crucial for development and respiration. Dysregulation can result in diabetes mellitus and related complications. In the current study, Erythrina suberosa sawdust-deposited manganese dioxide nanoparticles (MnO2 NPs) were used for colorimetric glucose detection. Sawdust-deposited MnO2 NPs were synthesized using Dalbergia sissoo extract and characterized with different analytical techniques such as XRD, FTIR, EDX, SEM, and UV–Vis spectrophotometer. Various functional groups in FTIR spectrum of MnO2 were reported such as –OH, Mn–O, and –OH coupled with Mn. XRD spectrum showed that the particles were in orthorhombic phase with a particle size of 38 nm. SEM analysis showed that the particles are dispersed homogenously on the surface of sawdust. EDX analysis showed the presence of various elements in the synthesized platform at different ratios. Color change from colorless to blue–green was noticed by the addition of glucose with the naked eye and analyzed confirmed by a UV–Vis spectrophotometer. To achieve optimum results, various parameters were optimized, such as nanoparticles loading, TMB concentration, pH, and incubation time. The proposed sensor's limit of detection and limit of quantification were calculated to be 1.8 × 10–8 M and 6.25 × 10–8 M, respectively, with a linear range of 1 × 10–9–3.6 × 10–7 M and an R2 value of 0.9992. The reaction time of the suggested sensor for glucose sensing was just 150 s. The proposed sensor has also been used for the detection of glucose in the urine samples of diabetic patients. [ABSTRACT FROM AUTHOR]

Highlights: A novel photoelectrochemical (PEC) photosensor composed of GaN nanowire-on-Si platform demonstrates record-high responsivity of 247.8 mA W−1 with ultra-stable operation characteristics. Strategic internal and external band structure engineering of semiconductor nanowires promotes efficient PEC reaction via controlling carrier dynamics while preserving nanowires from material degradation. The glucose sensing system is constructed to successfully analyze blood glucose levels in real human serum samples, featuring a high sensitivity of 0.173 µA µM−1 cm−2 and a low detection limit of 0.07 µM. Photosensors with versatile functionalities have emerged as a cornerstone for breakthroughs in the future optoelectronic systems across a wide range of applications. In particular, emerging photoelectrochemical (PEC)-type devices have recently attracted extensive interest in liquid-based biosensing applications due to their natural electrolyte-assisted operating characteristics. Herein, a PEC-type photosensor was carefully designed and constructed by employing gallium nitride (GaN) p–n homojunction semiconductor nanowires on silicon, with the p-GaN segment strategically doped and then decorated with cobalt–nickel oxide (CoNiOx). Essentially, the p–n homojunction configuration with facile p-doping engineering improves carrier separation efficiency and facilitates carrier transfer to the nanowire surface, while CoNiOx decoration further boosts PEC reaction activity and carrier dynamics at the nanowire/electrolyte interface. Consequently, the constructed photosensor achieves a high responsivity of 247.8 mA W−1 while simultaneously exhibiting excellent operating stability. Strikingly, based on the remarkable stability and high responsivity of the device, a glucose sensing system was established with a demonstration of glucose level determination in real human serum. This work offers a feasible and universal approach in the pursuit of high-performance bio-related sensing applications via a rational design of PEC devices in the form of nanostructured architecture with strategic doping engineering. [ABSTRACT FROM AUTHOR]

Ni3(HITP)2 (HITP: 2,3,6,7,10,11-hexaiminotriphenylene) is a very typical 2D electrically conductive metal–organic framework (EC-MOF) material with great promising as active materials in electronic devices. Gas–liquid interface self-assembly is a common method of processing free-standing thin films for this EC-MOF. Owing to the different contact environment during growth process, Ni3(HITP)2 film prepared by gas–liquid interface method has different morphology for up-side surface exposed to air and down-side surface infiltrated in solution. However, the asymmetrical morphology of Ni3(HITP)2 film and its influence on sensing performance have never been implemented. In this work, gas–liquid interface self-assembly method is used to obtain an asymmetrical Ni3(HITP)2 nanofilm in surface morphology with a flat up-side surface and an island-like down-side surface. The surface morphology of as-prepared film has a remarkable influence on the glucose sensing property. The island-like structure for down-side surface film exhibits more excellent glucose sensing performance because of its abundant crystal defect which play an important role in enhancing glucose catalytic oxidation capacity. [ABSTRACT FROM AUTHOR]

Non-enzymatic detection of glucose is important and is found useful not only in clinical settings but also for quality analysis in food and beverages industry. The fabrication of a good electrocatalyst demands for excellent activity, stability, and easy synthesis methods. Herein, a non-enzymatic glucose sensor has been constructed using Au nanoparticles decorated over Cu2O cubes (Cu2O/nAu) synthesized via a simple cost-effective microwave-assisted technique. The preliminary characterizations including UV–Vis spectroscopy (UV–Vis), Scanning electron microscopy, and Elemental mapping confirmed the formation of Au-decorated over the Cu2O cubes and proved gold nanoparticles were decorated over the cubic structure of the Cu2O. Furthermore, the fabricated Cu2O/nAu was applied for non-enzymatic glucose detection in 0.1 M KOH. The modified glassy carbon electrode of Cu2O/nAu (Cu2O/nAu/GCE) exhibited a linear range from 10 µM to 1 mM for glucose with a limit of detection of 1 µM. The as-developed glucose sensor demonstrates outstanding electrocatalytic activity for the oxidation of glucose with strong stability and high reproducibility. The practical applicability of the developed sensor for non-enzymatic glucose detection was demonstrated by studying artificial sweetener, and commercially available glucose drink. Thus, the as-developed Cu2O/nAu/GCE have the potential for the development of a sensor for analyzing glucose in food and beverages. A simple and non-enzymatic glucose sensor with Nano Au Decorated Hybrid Cu2O cubes is demonstrated. The sensor exhibited a linear range from 10 µM to 1 mM for glucose with a limit of detection of 1 µM. The practical applicability was demonstrated with commercially available glucose drink and artificial sweetener [ABSTRACT FROM AUTHOR]

Aims/hypothesis: The brain is a major consumer of glucose as an energy source and regulates systemic glucose as well as energy balance. Although glucose transporters such as GLUT2 and sodium−glucose cotransporter 2 (SGLT2) are known to regulate glucose homeostasis and metabolism, the identity of a receptor that binds glucose to activate glucose signalling pathways in the brain is unknown. In this study, we aimed to discover a glucose receptor in the mouse hypothalamus. Methods: Here we used a high molecular mass glucose–biotin polymer to enrich glucose-bound mouse hypothalamic neurons through cell-based affinity chromatography. We then subjected the enriched neurons to proteomic analyses and identified adhesion G-protein coupled receptor 1 (ADGRL1) as a top candidate for a glucose receptor. We validated glucose–ADGRL1 interactions using CHO cells stably expressing human ADGRL1 and ligand–receptor binding assays. We generated and determined the phenotype of global Adgrl1-knockout mice and hypothalamus-specific Adgrl1-deficient mice. We measured the variables related to glucose and energy homeostasis in these mice. We also generated an Adgrl1Cre mouse model to investigate the role of ADGRL1 in sensing glucose using electrophysiology. Results: Adgrl1 is highly expressed in the ventromedial nucleus of the hypothalamus (VMH) in mice. Lack of Adgrl1 in the VMH in mice caused fasting hyperinsulinaemia, enhanced glucose-stimulated insulin secretion and insulin resistance. In addition, the Adgrl1-deficient mice had impaired feeding responses to glucose and fasting coupled with abnormal glucose sensing and decreased physical activity before development of obesity and hyperglycaemia. In female mice, ovariectomy was necessary to reveal the contribution of ADGRL1 to energy and glucose homeostasis. Conclusions/interpretation: Altogether, our findings demonstrate that ADGRL1 binds glucose and is involved in energy as well as glucose homeostasis in a sex-dependent manner. Targeting ADGRL1 may introduce a new class of drugs for the treatment of type 2 diabetes and obesity. [ABSTRACT FROM AUTHOR]

This paper focuses on designing a simple photonic crystal fiber (PCF) biosensor. The proposed glucose sensor is modelled by Lumerical software using the finite element method. To evaluate the efficiency of this model, different sensing properties such as birefringence, coupling length, and relative sensitivity are calculated at different air-filling fractions. The principle of this PCF is to detect the variations in the refractive index of the different concentration glucose solutions. The analyte will be injected into an elliptical channel surrounded by two rings of air holes in a hexagonal shape. Numerical simulations show that increasing the air-filling fraction yields high performance and more light confinement. At the air-filling fraction of 0.45, the maximum birefringence and relative sensitivity were 4.01 × 10−3 and 91%, respectively. Also, the coupling length reaches a minimum of 162.09 μm. [ABSTRACT FROM AUTHOR]

Gold nanomaterials possess leading interest in the field of nanomaterials due to their vast applications both in advanced chemical and medicinal industries. Gold nanorods (AuNRs) were synthesized via a seed-mediated growth approach for catalytic and electrocatalytic applications. UV–vis absorption spectroscopy and scanning electron microscopy were employed to characterize AuNRs. The focus was to achieve AuNRs of high aspect ratios and good yield. For anisotropic AuNRs, two plasmon peaks are observed; transverse and longitudinal peaks. In the synthesis process, morphology of the gold nanorods was tuned varying the pH of the solution ranges from 3.45 to 1.6. By varying the pH, gold nanorods of different aspect ratios were obtained. Gold nanorods with the aspect ratio of 7.5 containing maximum amount of nitric acid and a pH value of 1.6 revealed the most stability. Catalytic applications were monitored by degradation of an organic pollutant. The degradation percentages of 98% were achieved at 12 min duration. Non-enzymatic electrochemical glucose sensor was fabricated via glassy carbon electrode modification with gold nanorods and studied using cyclic voltammetry. All samples showed good electrochemical response. Among all samples, the one with maximum amount of nitric acid and a pH value of 1.6 revealed the most stability and high sensitivity for glucose sensing. [ABSTRACT FROM AUTHOR]

Organic electrochemical transistors (OECTs) have been hailed as highly sensitive biomolecular sensors among organic electronic devices due to their superior stability in an aqueous environment and high transconductance. At the same time, plasmon based sensors are known to provide high sensitivity for biosensing due to the highly localized plasmonic field. Here we report a plasmonic OECT (POET) device that synchronizes the advantages of OECTs and plasmonic sensors on a single platform. The platform is fabricated by a simple, cost-effective, and high-throughput nanoimprinting process, which allows plasmonic resonance peak tuning to a given visible wavelength of interest for versatile biosensing. With glucose sensing as proof, a five-times sensitivity enhancement is obtained for POET compared to a regular (non-plasmonic) OECT. Thus, the POET paves the way to a new paradigm of optoelectronic sensors that combines the inherent high sensitivity of OECTs and localized plasmonic field to sense a vast realm of biomolecules. [ABSTRACT FROM AUTHOR]

Accurate and rapid detection of the concentration of glucose in the blood is crucial in disease prevention and detection. Monolithic nanoporous silver (np-Ag) with a controllable dimension and thickness is prepared in this study through the electrochemical growth/reduction of AgCl films on silver substrates. With this film as a substrate, a Ni(OH)2/np-Ag composite material is prepared with the electrodeposition method. Scanning electron microscopy, X-ray photoelectron spectroscopy, and X-ray diffraction analysis are applied to characterise the morphology and composition of the Ni(OH)2/np-Ag materials. Results show that np-Ag has a monolithic porous structure, and Ni(OH)2 is generated above np-Ag. The composite material has an average size of 100 nm. Cyclic voltammetry and amperometric measurements are used to study the catalytic oxidation behaviour of glucose in 0.1 M NaOH solution. The composite material exhibits high catalytic activity for the electrochemical oxidation of glucose and has excellent sensitivity (0.21935 mA μmol L−1 cm−2) and detection capability (the lowest detection limit is 0.1425 μmol L−1 (S/N = 3)). [ABSTRACT FROM AUTHOR]

Glucose measurement is one of the essential health monitoring practices for maintaining blood sugar levels. Here, we have fabricated a highly specific capacitive nano-sensor for non-enzymatic glucose detection. Capacitance measurements were carried out on polyvinyl alcohol capped copper oxide (PVA-CuO) thin films on indium tin oxide (ITO) coated glass using ARDUINO UNO. The capacitance study shows a decrease in capacitance with an increase in glucose concentrations. The applicability in real samples was performed by studying the glucose in the presence of fetal bovine serum. Most commonly found interfering agents were used for interference studies, which confirmed the capacitive nano-sensor specificity. The system was further checked for repeatability up to six readings and reproducibility up to 5 chips. The shelf-life study showed stability for four weeks of a chip. These studies indicate that this capacitance-based measurement unit can be used for reliable, rapid, and non-enzymatic detection of glucose in real sample. [ABSTRACT FROM AUTHOR]

In this work, a convenient, low cost and fast detection of glucose (GO) in human blood has been investigated. For this purpose, a non-enzymatic sensor based on the hydrothermally prepared cobalt hydroxide nano-catalyst was fabricated and used for analysis of GO level in biological fluids. The electrochemical ability of the modified glassy carbon electrode (GCE) for GO measuring was studied by cyclic voltammetry and chronoamperometry assays. The chronoamperometric data indicate that the proposed sensing platform is capable of measuring changes in GO levels within a linear range of 1.5–460 µM and low detection limit of 0.8 µM. The cobalt hydroxide modified GCE depicts a significant resistant versus common interfering species such as fructose, cholesterol, ascorbic acid, l-cysteine and uric acid. In addition, the suggested GO sensor was employed for determination of analyte concentration in blood samples from athletes. This novel platform is characterized by its low price, simple operation, high anti-interference property and high sensitivity. The experimental results proved that the cobalt hydroxide modified GCE is an effective strategy for non-enzymatic GO detection in clinical applications.Graphical Abstract: In this work, a convenient, low cost and fast detection of glucose (GO) in human blood has been investigated. For this purpose, a non-enzymatic sensor based on the hydrothermally prepared cobalt hydroxide nano-catalyst was fabricated and used for analysis of GO level in biological fluids. The electrochemical ability of the modified glassy carbon electrode (GCE) for GO measuring was studied by cyclic voltammetry and chronoamperometry assays. The chronoamperometric data indicate that the proposed sensing platform is capable of measuring changes in GO levels within a linear range of 1.5–460 µM and low detection limit of 0.8 µM. The cobalt hydroxide modified GCE depicts a significant resistant versus common interfering species such as fructose, cholesterol, ascorbic acid, l-cysteine and uric acid. In addition, the suggested GO sensor was employed for determination of analyte concentration in blood samples from athletes. This novel platform is characterized by its low price, simple operation, high anti-interference property and high sensitivity. The experimental results proved that the cobalt hydroxide modified GCE is an effective strategy for non-enzymatic GO detection in clinical applications. [ABSTRACT FROM AUTHOR]

In this work, vertically aligned nanosheets of manganese oxide (MnO2) were deposited on stainless steel (SS) substrate via binder free anodic electrodeposition method. The MnO2 films were characterized with X-ray diffraction, energy dispersive X-ray spectroscopy, field emission scanning electron microscopy and X-ray photoelectron spectroscopy to study the crystal structure, elemental composition, morphology and chemical state. Further, the films were explored as an electrode for electrochemical detection of glucose by cyclic voltammetry and i–t amperometric techniques using three electrode system. The sensitivity of 4341 µA mM−1 cm−2 at working potential of 0.5 V/SCE was shown by MnO2 electrode with wide linear range of 50 µM–1.2 mM having lower detection limit of 0.53 µM. This result points that the vertically aligned nanosheets of MnO2 thin film can be a promising candidate for enzymeless glucose sensing. [ABSTRACT FROM AUTHOR]

A multi-shelled NiO hollow sphere was synthesized by a facile glucose-mediated hydrothermal route. The carbonaceous microsphere was utilized as a sacrificial template for the formation of multi-shells. All the shells were formed by a single pyrolysis step. The multi-shelled hollow sphere can provide enhanced active surface area and additional reactive sites, which facilitate faster ion intercalation and deintercalation, and play key roles in electrochromic devices and sensing application, including glucose sensing. Herein, we employed the as-synthesized material for electrochromic devices. As expected, NiO multi-shelled hollow microspheres exhibit a superior transmission modulation (ΔT = 47%) and yield a coloration efficiency of ~ 85.3 cm2 C−1, which is ~ 2.37 times higher than that of NiO microflakes which was synthesized in the absence of glucose. The geometry of the self-supported multi-shelled architecture ensures that the active faradaic sites can be in intimate contact with the electrolyte to enhance ionic diffusion. The observed colored and bleached switching time of multi-shelled hollow sphere is 6.7 s and 2.7 s respectively. A quasi-solid-state electrochromic device is also displayed with the aid of gel electrolyte with reversible color change from dark brown to transparent. Furthermore, the multi-shelled NiO displayed excellent catalytic activity towards non-enzymatic glucose sensing with a high sensitivity of 1646 ± 5 μA cm−2 mM−1 over a linear range of 2 μM–2.6 mM with a lowest detection limit of 1.5 ± 0.2 μM. Analysis on blood serum as a real biological sample reflects the practicability of the fabricated sensor. Developing hollow structured multi-shelled materials based on metal oxides will pave the way to design advanced electrode materials for electrochromic smart windows and non-enzymatic glucose sensors. [ABSTRACT FROM AUTHOR]

Renal complications are long-term effect of diabetes mellitus where glucose is excreted in urine. Therefore, reliable glucose detection in urine is critical. While commercial urine strips offer a simple way to detect urine sugar, poor sensitivity and low reliability limit their use. A hybrid glucose oxidase (GOx)/horseradish peroxidase (HRP) assay remains the gold standard for pathological detection of glucose. A key restriction is poor stability of HRP and its suicidal inactivation by hydrogen peroxide, a key intermediate of the GOx-driven reaction. An alternative is to replace HRP with a robust inorganic enzyme-mimic or NanoZyme. While colloidal NanoZymes show promise in glucose sensing, they detect low concentrations of glucose, while urine has high (mM) glucose concentration. In this study, a free-standing copper NanoZyme is used for the colorimetric detection of glucose in human urine. The sensor could operate in a biologically relevant dynamic linear range of 0.5–15 mM, while showing minimal sample matrix effect such that glucose could be detected in urine without significant sample processing or dilution. This ability could be attributed to the Cu NanoZyme that for the first time showed an ability to promote the oxidation of a TMB substrate to its double oxidation diimine product rather than the charge-transfer complex product commonly observed. Additionally, the sensor could operate at a single pH without the need to use different pH conditions as used during the gold standard assay. These outcomes outline the high robustness of the NanoZyme sensing system for direct detection of glucose in human urine. [ABSTRACT FROM AUTHOR]

Polyaniline nanoskein (PANS), which have polyaniline nanofibers, was developed. PANS was formulated via sequential extracting, heating, and swelling processes. The compositions of PANS have been analyzed using X-ray photoelectron spectroscopy, Fourier transform infrared spectroscopy, thermogravimetric analysis, and Brunauer–Emmett–Teller analysis, and the results of which indicate that PANS is composed of solely organic materials. Moreover, PANS has been shown convertible absorbance characteristics according to surrounding acidic environments, and using these characteristics, the possibility of PANS for sensing of surrounding redox state changes is presented. [ABSTRACT FROM AUTHOR]

Among the so-called non-conventional yeasts, Kluyveromyces marxianus has extremely potent traits that are suitable for industrial applications. Indeed, it has been used for the production of various enzymes, chemicals, and macromolecules in addition to utilization of cell biomass as nutritional materials, feed and probiotics. The yeast is expected to be an efficient ethanol producer with advantages over Saccharomyces cerevisiae in terms of high growth rate, thermotolerance and a wide sugar assimilation spectrum. Results of comprehensive analyses of its genome and transcriptome may accelerate studies for applications of the yeast and may further increase its potential by combination with recent biotechnological tools including the CRISPR/Cas9 system. We thus review published studies by merging with information obtained from comprehensive data including genomic and transcriptomic data, which would be useful for future applications of K. marxianus. [ABSTRACT FROM AUTHOR]

Boronic acid-doped carbon nanoparticles were prepared and are shown to undergo aggregation induced emission (AIE). The nanoparticle composite is a viable fluorescent probe for glucose determination by using the RGB technique and a smartphone. The structure and the chemical composition of the doped carbon nanoparticles were confirmed by SEM, TEM, FTIR and UV-vis spectroscopy. The combination of 4-carboxyphenylboronic acid with o-phenylenediamine and rhodamine B endowed the hybrid with high fluorescence intensity (quantum yield 46%). Compared with conventional two-step preparation of boronic acid-based fluorescent probes for glucose, the present one step synthesis strategy is simpler and more effective. The addition of glucose causes the formation of covalent bonds between the cis-diols group of glucose molecules and boronic acid moiety. Fluorescent intensity can be quantified using dual wavelengths simultaneously, where both increases, as the target analytes bind to the bronic acid. These variations was monitored by the smartphone camera, and the green channel intensities of the colored images were processed by using the RGB option of a smartphone. The assay works in the 32 μM to 2 mM glucose concentration range and has an 8 μM detection limit. The method was successfully used for the assay of glucose in diluted human serum. [ABSTRACT FROM AUTHOR]

Our data proposes that glucose is transferred directly to the cerebrospinal fluid (CSF) of the hypothalamic ventricular cavity through a rapid "fast-track-type mechanism" that would efficiently stimulate the glucosensing areas. This mechanism would occur at the level of the median eminence (ME), a periventricular hypothalamic zone with no blood-brain barrier. This "fast-track" mechanism would involve specific glial cells of the ME known as β2 tanycytes that could function as "inverted enterocytes," expressing low-affinity glucose transporters GLUT2 and GLUT6 in order to rapidly transfer glucose to the CSF. Due to the large size of tanycytes, the presence of a high concentration of mitochondria and the expression of low-affinity glucose transporters, it would be expected that these cells accumulate glucose in the endoplasmic reticulum (ER) by sequestering glucose-6-phosphate (G-6-P), in a similar way to that recently demonstrated in astrocytes. Glucose could diffuse through the cells by micrometric distances to be released in the apical region of β2 tanycytes, towards the CSF. Through this mechanism, levels of glucose would increase inside the hypothalamus, stimulating glucosensing mechanisms quickly and efficiently. Key messages: • Glucose diffuses through the median eminence cells (β2 tanycytes), towards the hypothalamic CSF. • Glucose is transferred through a rapid "fast-track-type mechanism" via GLUT2 and GLUT6. • Through this mechanism, hypothalamic glucose levels increase, stimulating glucosensing. [ABSTRACT FROM AUTHOR]

Schiff-bases of metformin with each of salicylaldehyde (HL1); 2,3-dihydroxybenzaldehyde (H2L2); 2,4-dihydroxybenzaldehyde (H2L3); 2,5-dihydroxybenzaldehyde (H2L4); 3,4-dihydroxybenzaldehyde (H2L5) and 2-hydroxynaphthaldehyde (HL6) and their complexes with Pr(III) were synthesized by template reaction. The complexes were characterized through elemental analysis, conductivity and magnetic moment measurements, IR, UV-Vis., fluorescence, GC-MS and XRD spectroscopy. The complexes exhibit a series of characteristic emission bands for Pr3+ ion in the 481-472 and 590-580 nm range with a 318-332 nm excitation source. The complexes have eight coordinated structure with the formulae [PrL1-4,6(NO3)2(H2O)3].nH2O where n = 1, 1½, 3, 4, 4 and [PrL5(NO3)(H2O)5].2H2O. The suggested stereochemistry was confirmed using TGA, DTG and DTA analysis and a mechanism for thermal decomposition was proposed. Coates-Redfern equation was used to calculate kinetic and thermodynamic parameters of the main decomposition step. The utility of the complexes towards the detection of glucose at physiologically relevant pH in phosphate buffer using UV-Vis and fluorescence spectroscopy as well as viscosity measurements are tried where the association constants were calculated. [ABSTRACT FROM AUTHOR]

Optical monitoring of blood glucose levels for non-invasive diagnosis is a growing area of research. Recent efforts in this direction have been inclined towards reducing the requirement of calibration framework. Here, we are presenting a systematic investigation on the influence of variation in the ratio of calibration and validation points on the prospective predictive accuracy of spectral models. A fiber-optic probe coupled Raman system has been employed for transcutaneous measurements. Limit of agreement analysis between serum and partial least square regression predicted spectroscopic glucose values has been performed for accurate comparison. Findings are suggestive of strong predictive accuracy of spectroscopic models without requiring substantive calibration measurements.Graphical abstract [ABSTRACT FROM AUTHOR]

This work reports the substrate temperature-influenced change in the structural, morphological, optical, and glucose sensing properties of silver (Ag) nanoparticles (NPs) deposited on p-type Si (100) wafers. AgNP films grown at temperatures ranging from RT to 600 °C clearly show a dependence of orientation texture and surface morphology on substrate temperature (Ts). As Ts increases from RT towards 600 °C, the preferred orientation of AgNP film changes from (111) to (200). The AgNPs size, that is Ts-dependent, reaches the maximum value at Ts = 300 °C. This result is attributed to restructuring of AgNPs texture. Moreover, the AgNP shape also changes from ellipsoid to sphere as Ts increases from RT to 600 °C. Surface plasmon enhancement in photoluminescence intensity is observed with increase in Ts. It is found also that the AgNP film deposited at 300 °C has considerable reflectance reduction relative to the silicon substrate, in wavelength range of 300-800 nm and a progressive red shift of localized surface plasmon resonances caused by the adding of increasing quantities of glucose has been observed. As a proof of concept, we also demonstrate the capability of grown AgNP substrates for glucose detection based on surface enhanced Raman spectroscopy in physiological concentration range with short integration time 10 s, varying with Ts. [ABSTRACT FROM AUTHOR]

We develop a unique ternary Pd-Ni-P nanocatalyst for the sensitive enzymefree electrooxidation detection of glucose under alkaline conditions. By reducing the distance between the Pd and Ni active sites in the Pd-Ni-P nanoparticles (NPs) via atom engineering, the catalyst structure is transformed from Pd@Ni-P dumbbells into spherical NPs, greatly enhancing the catalyst sensitivity. The glassy carbon electrode modified with Pd-Ni-P ternary NPs, which behaves as an efficient nonenzymatic glucose sensor, offers excellent electrocatalytic performance with a high sensitivity of 1,136 μA·mM·cm, a short response time of 2 s, a wide linear range of 0.5 μM to 10.24 mM, a low limit of detection of 0.15 μM (signal-to-noise ratio = 3), and good selectivity and reproducibility. Moreover, owing to its superior catalytic performance, the Pd-Ni-P modified electrode has excellent reliability for glucose detection in real samples of human serum. Our study provides a promising alternative strategy for designing and constructing high-performance multicomponent nanocatalyst-based sensors. [ABSTRACT FROM AUTHOR]

The hypothalamic feeding center plays an important role in energy homeostasis. The feeding center senses the systemic energy status by detecting hormone and nutrient levels for homeostatic regulation, resulting in the control of food intake, heat production, and glucose production and uptake. The concentration of glucose is sensed by two types of glucose-sensing neurons in the feeding center: glucose-excited neurons and glucose-inhibited neurons. Previous studies have mainly focused on glucose metabolism as the mechanism underlying glucose sensing. Recent studies have indicated that receptor-mediated pathways also play a role in glucose sensing. This review describes sweet taste receptors in the hypothalamus and explores the role of sweet taste receptors in energy homeostasis. [ABSTRACT FROM AUTHOR]

We have developed a non-enzymatic fluorescent biosensor for glucose sensing based on ZnO nanorods. ZnO nanorods of high density, high crystallinity, and good alignment were grown on low-cost industrial copper substrates at low temperature. To grow them directly on the substrates without using a seed layer, we utilized a simple one-step seedless hydrothermal method, which is based on galvanic cell structure. Herein, the glucose-treated ZnO nanorods together with the ultraviolet (UV) irradiation of the sample during the photoluminescent measurement played the role of a catalyst. They decomposed glucose into hydrogen peroxide (HO) and gluconic acid, which is similar to the glucose oxidase enzyme (GOx) used in enzymatic sensors. Due to the formation of HO, the photoluminescence intensity of the UV emission peak of ZnO nanorods decreased as the glucose concentration increased from 1 mM to 100 mM. In comparison with glucose concentration of a normal human serum, which is in the range of 4.4-6.6 mM, the obtained results show potential of non-enzymatic fluorescent biosensors in medical applications. [ABSTRACT FROM AUTHOR]

Morphology of different CuO nanostructures is controlled by changing the precursor counterions. The CuO nanostructures were synthesized using three different precursor salts of copper namely acetate, nitrate, and sulfate via facile chemical precipitation route. The synthesized CuO nanostructures were thoroughly characterized using X-ray diffraction, optical spectroscopy, electron microscopy etc. The nanostructures were studied for catalytic nonenzymatic glucose sensing applications. CuO nanostructures synthesized from copper sulfate having flower-like morphology showed the highest glucose sensitivity of 1830 μAmMcm in a linear range of 0.01-0.2 mM with a detection limit of 8 μM. [ABSTRACT FROM AUTHOR]

The hypothesis of fetal origins of adult disease states that early life events program the occurrence of significant adult diseases, including diabetes and obesity. Maternal diabetes is associated with general stress environment for developing fetus, and gestational diabetes is an independent risk factor for type 2 diabetes and metabolic syndrome in offspring. Intra-uterine fetal programming of fetal tissues exposes the offspring to increased risk of impaired glucose tolerance, type 2 diabetes, and cardiovascular disease. Here, we examined the transmission of maternal diabetes-induced fetal programming in second generation and compared maternal and paternal routes of intergenerational effects. We organized 40 Wistar rats into three groups, male offspring of diabetic mothers, female offspring of diabetic mothers, and offspring of control mothers. These groups were mated with normal healthy rats to assess the effect of grand-maternal diabetes on pregnancy outcome in F2 rats, as well as glucose-sensing parameters, insulin resistance, and glucose tolerance prenatally and postnatally. We found that F2 offspring of diabetic mothers had impaired glucose sensing, increased oxidative stress, insulin resistance, and impaired glucose tolerance, and these effects were more prominent in the F2 offspring of F1 female rats (F2-DF1F). We deduce that fetal programming of maternal diabetes is mostly transmitted through maternal line across two generations. [ABSTRACT FROM AUTHOR]

Transgenerational inheritance of various diseases and phenotypes has been demonstrated in diverse species and involves various epigenetic markers. Obesity and malnourishment are nutritional stresses that have effects on offspring through increasing their risk of diabetes and/or obesity. Obesity and malnourishment both affect glucose metabolism and alter oxidative stress parameters in key organs. We induced obesity and malnutrition in F0 female rats by the use of obesogenic diet and protein-deficient diet, respectively. F0 obese and malnourished females were mated with control males and their offspring (F1 generation) were maintained on control diets. The male and female F1 offspring were mated with controls and the resultant offspring (F2 generation) were maintained on control diet. Glucose-sensing markers, glucose metabolism, indicators of insulin resistance and oxidative stress parameters were assessed during fetal development and till the adulthood of the offspring. Glucose-sensing genes were significantly over-expressed in distinct fetal tissues of F2 offspring of malnourished F1 females (F2-MF1F), specifically in fetal pancreas, liver, and adipose tissue. Nuclear and mitochondrial 8-oxo-dG DNA content was significantly elevated in F2-MF1F fetal pancreas. Maternal FBG was significantly elevated in F2-MF1F and F2 offspring of obese F1 females (F2-OF1F) during pregnancy. Males and females offspring of F2-OF1 exhibited significantly elevated FBG and impaired OGTT. Offspring of F2-MF1F showed similar results, while that of F2-MF1M did not significantly deviate from controls. F2-OF1F and F2-MF1F offspring exhibited significant deviation in insulin levels and HOMA-IR levels from controls. Malnourishment has a stronger transgenerational effect through maternal line compared to obesity and malnourishment through paternal line in increasing risk of diabetes in F2 generation. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a chronic metabolic disorder, requiring vigilant monitoring of blood glucose levels. In this study, an injectable fluorescent enzymatic hydrogel was designed for rapid glucose detection. The leakage-free glucose-responsive hydrogel was constructed by the covalent linkage of a multi-arm poly-(ethylene glycol) (PEG), bovine serum albumin (BSA), glucose oxidase (GOx), and 4-(aminomethyl)-6,7-dimethoxycoumarin (Coumarin-NH). The GOx serves as glucose-recognition element and the pH-sensitive Coumarin-NH as a fluorescence turn-on reporter. The material properties of the fluorescent hydrogel were systematically characterized which show high elasticity with good mechanical strength. Upon the addition of glucose, the as-developed fluorescent hydrogel shows a fast response time, good sensitivity, and good reproducibility at physiological pH and ambient temperature. The glucose-sensing mechanism is based on the oxidation of the glucose by GOx that generates protons to change the local pH. Consequently, protonation of the covalently immobilized and pH-sensitive Coumarin-NH turns on the fluorescence of the coumarin. The fluorescence hydrogel developed holds great promise as an injectable, implantable glucose-sensing biomaterials for in vivo continuous glucose monitoring. [ABSTRACT FROM AUTHOR]

The glucose transporter isoform GLUT2 is expressed in liver, intestine, kidney and pancreatic islet beta cells, as well as in the central nervous system, in neurons, astrocytes and tanycytes. Physiological studies of genetically modified mice have revealed a role for GLUT2 in several regulatory mechanisms. In pancreatic beta cells, GLUT2 is required for glucose-stimulated insulin secretion. In hepatocytes, suppression of GLUT2 expression revealed the existence of an unsuspected glucose output pathway that may depend on a membrane traffic-dependent mechanism. GLUT2 expression is nevertheless required for the physiological control of glucose-sensitive genes, and its inactivation in the liver leads to impaired glucose-stimulated insulin secretion, revealing a liver-beta cell axis, which is likely to be dependent on bile acids controlling beta cell secretion capacity. In the nervous system, GLUT2-dependent glucose sensing controls feeding, thermoregulation and pancreatic islet cell mass and function, as well as sympathetic and parasympathetic activities. Electrophysiological and optogenetic techniques established that Glut2 (also known as Slc2a2)-expressing neurons of the nucleus tractus solitarius can be activated by hypoglycaemia to stimulate glucagon secretion. In humans, inactivating mutations in GLUT2 cause Fanconi-Bickel syndrome, which is characterised by hepatomegaly and kidney disease; defects in insulin secretion are rare in adult patients, but GLUT2 mutations cause transient neonatal diabetes. Genome-wide association studies have reported that GLUT2 variants increase the risks of fasting hyperglycaemia, transition to type 2 diabetes, hypercholesterolaemia and cardiovascular diseases. Individuals with a missense mutation in GLUT2 show preference for sugar-containing foods. We will discuss how studies in mice help interpret the role of GLUT2 in human physiology. [ABSTRACT FROM AUTHOR]

Maternal diabetes can induce permanent changes in glucose homeostasis that can occur pre- and post-natal and leads to type 2 diabetes in adulthood. This study aimed to investigate the effect of maternal diabetes on the F1 offspring peripheral glucose sensing and mitochondrial biogenesis in an attempt to clarify the mechanism of diabetogenic programming. Two groups of female Wistar rats were used (diabetic and control); diabetes was neonatally induced by STZ injection to 5-day old rats. After the pregnancy and delivery, the offspring were weaned to control diet or high-caloric (HCD) diet and followed up for 30 weeks. Every 5 weeks, OGTT was constructed, and serum and tissues were obtained for the assessment of mTFA, mtDNA, UCP2, insulin receptor (IR), phospho-insulin receptor (phospho-IR), and GLUT4. The result indicated impaired glucose tolerance (IGT) and insulin resistance in the offspring under control diet at the 15th week of age and thereafter while those offspring under HCD showed IGT at 10th week, and diabetes was evidenced at the 25th week of age. This defect in glucose metabolism was preceded by impairment in the phosphorylation of IR and decreased IR and Glut4 that cause impaired glucose sensing together with inhibited mitochondrial biogenesis in muscle and adipose tissues. This study indicated that maternal diabetes caused impaired glucose sensing and insulin resistance in the peripheral tissues and caused change in the expression of genes involved in mitochondrial biogenesis and function. Post-natal feeding with HCD may accelerate these changes. Male F1 offspring appears to be more sensitive than females for fetal programming of T2D. [ABSTRACT FROM AUTHOR]

The MYB-like gene AtGGS1 ( A rabidopsis t haliana G A and g lucose s ignaling) is a DELLA target gene, and also a component of the HXK1 transcriptional complex, implying its roles in gibberellic acid (GA) and glucose signaling. We evaluated the function of AtGGS1 through genetic and biochemical approaches. We conducted phenotypic analyses of the null mutant of AtGGS1 ( atggs1), an AtGGS1 overexpression lines (O/E), and RNA interference (RNAi) lines. The results showed that AtGGS1 inhibited seed germination, root elongation, and leaf expansion. The O/E line flowered earlier and accumulated less chlorophyll than did wild type. The transcript levels of genes encoding GA signaling components, photosynthetic proteins, and glucose sensors and transporters differed among atggs1, O/E, and RNAi lines, as determined by quantitative polymerase chain reaction analyses. AtGGS1 repressed the expression of GNL, which encodes an important player integrating the signaling networks of nutrients (nitrate and glucose) and phytohormones (GA, cytokinin). Genetic and chromatin immunoprecipitation experiments showed that GNL is the direct target of AtGGS1. Our results show that although both AtGGS1 and GNL are downstream of the DELLA/PIF transcription complex and are repressors of GA signaling, AtGGS1 directly regulates the expression of GNL in GA and glucose signaling. [ABSTRACT FROM AUTHOR]

The hepatic glucose-sensing system is a functional network of enzymes and transcription factors that is critical for the maintenance of energy homeostasis and systemic glycemia. Here we review the recent literature on its components and metabolic actions. Glucokinase (GCK) is generally considered as the initial postprandial glucose-sensing component, which acts as the gatekeeper for hepatic glucose metabolism and provides metabolites that activate the transcription factor carbohydrate response element binding protein (ChREBP). Recently, liver receptor homolog 1 (LRH-1) has emerged as an upstream regulator of the central GCK-ChREBP axis, with a critical role in the integration of hepatic intermediary metabolism in response to glucose. Evidence is also accumulating that O-linked β- N-acetylglucosaminylation ( O-GlcNAcylation) and acetylation can act as glucose-sensitive modifications that may contribute to hepatic glucose sensing by targeting regulatory proteins and the epigenome. Further elucidation of the components and functional roles of the hepatic glucose-sensing system may contribute to the future treatment of liver diseases associated with deregulated glucose sensors. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Acute systemic delivery of the sulfonylurea receptor (SUR)-1-specific ATP-sensitive K channel (K) opener, NN414, has been reported to amplify glucose counter-regulatory responses (CRRs) in rats exposed to hypoglycaemia. Thus, we determined whether continuous NN414 could prevent hypoglycaemia-induced defective counter-regulation. Methods: Chronically catheterised male Sprague-Dawley rats received a continuous infusion of NN414 into the third ventricle for 8 days after implantation of osmotic minipumps. Counter-regulation was examined by hyperinsulinaemic-hypoglycaemic clamp on day 8 after three episodes of insulin-induced hypoglycaemia (recurrent hypoglycaemia [RH]) on days 5, 6 and 7. In a subset of rats exposed to RH, NN414 infusion was terminated on day 7 to wash out NN414 before examination of counter-regulation on day 8. To determine whether continuous NN414 exposure altered K function, we used the hypothalamic glucose-sensing GT1-7 cell line, which expresses the SUR-1-containing K channel. Results: Continuous exposure to NN414 in the setting of RH increased, rather than decreased, the glucose infusion rate (GIR), as exemplified by attenuated adrenaline (epinephrine) secretion. Termination of NN414 on day 7 with subsequent washout for 24 h partially diminished the GIR. The same duration of exposure of GT1-7 cells to NN414 substantially reduced K conductance, which was also reversed on washout of the agonist. The suppression of K current was not associated with reduced channel subunit mRNA or protein levels. Conclusions/interpretation: These data indicate that continuous K activation results in suppressed CRRs to hypoglycaemia in vivo, which in vitro is associated with the reversible conversion of K into a stable inactive state. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Hypothalamic glucose-excited (GE) neurons contribute to whole-body glucose homeostasis and participate in the detection of hypoglycaemia. This system appears defective in type 1 diabetes, in which hypoglycaemia commonly occurs. Unfortunately, it is at present unclear which molecular components required for glucose sensing are produced in individual neurons and how these are functionally linked. We used the GT1-7 mouse hypothalamic cell line to address these issues. Methods: Electrophysiological recordings, coupled with measurements of gene expression and protein levels and activity, were made from unmodified GT1-7 cells and cells in which AMP-activated protein kinase (AMPK) catalytic subunit gene expression and activity were reduced. Results: Hypothalamic GT1-7 neurons express the genes encoding glucokinase and ATP-sensitive K channel (K) subunits K 6.2 and Sur1 and exhibit GE-type glucose-sensing behaviour. Lowered extracellular glucose concentration hyperpolarised the cells in a concentration-dependent manner, an outcome that was reversed by tolbutamide. Inhibition of glucose uptake or metabolism hyperpolarised cells, showing that energy metabolism is required to maintain their resting membrane potential. Short hairpin (sh)RNA directed to Ampkα2 (also known as Prkaa2) reduced GT1-7 cell AMPKα2, but not AMPKα1, activity and lowered the threshold for hypoglycaemia-induced hyperpolarisation. sh Ampkα1 (also known as Prkaa1) had no effect on glucose-sensing or AMPKα2 activity. Decreased uncoupling protein 2 ( Ucp2) mRNA was detected in AMPKα2-reduced cells, suggesting that AMPKα2 regulates UCP2 levels. Conclusions/interpretation: We have demonstrated that GT1-7 cells closely mimic GE neuron glucose-sensing behaviour, and reducing AMPKα2 blunts their responsiveness to hypoglycaemic challenge, possibly by altering UCP2 activity. These results show that suppression of AMPKα2 activity inhibits normal glucose-sensing behaviour and may contribute to defective detection of hypoglycaemia. [ABSTRACT FROM AUTHOR]

Thermoresponsive microgels have been shown to be an excellent platform for designing sensor materials. Recently, poly ( N-isopropylacrylamide)- co-acrylic acid (pNIPAm- co-AAc) microgel based etalon materials have been described as direct sensing materials that can be designed to have a single, unique color. These color tunable materials show immense promise for sensing due to their spectral sensitivity and bright visual color. Here, we describe a proof-of-concept for etalon sensing of glucose. We found that aminophenylboronic acid (APBA)-functionalized pNIPAm- co-AAc microgels in an etalon respond to 3 mg/mL glucose concentrations by red shifting their reflectance peaks by 110 nm up to 150 nm. Additionally, APBA-functionalized pNIPAm- co-AAc microgels have a depressed volume phase transition temperature at 18-20 °C, which shifts to 24-26 °C after glucose binding. We also demonstrate that these materials show a marked visual color change, which is a first step towards developing direct read-out sensor devices. [Figure not available: see fulltext.] [ABSTRACT FROM AUTHOR]

Silicon nitride microring resonators were demonstrated as chemical sensors. The microring devices, with diameter of 100 μm, were fabricated using complementary metal oxide semiconductor (CMOS)-compatible technology, and a high Q factor of 15000 was realized with free spectrum range (FSR) of 2 nm. The structures were further packaged to perform as chemical sensors, and their functionality was proved using deionized water (DI water) and ethanol as detecting mediums. Lastly, the packaged chips were used to detect glucose solutions with various concentrations, and a detection capability of refractive index change of 10−3 refractive index unit (RIU) was obtained. [ABSTRACT FROM AUTHOR]

The control of body weight and of blood glucose concentrations depends on the exquisite coordination of the function of several organs and tissues, in particular the liver, muscle and fat. These organs and tissues have major roles in the use and storage of nutrients in the form of glycogen or triglycerides and in the release of glucose or free fatty acids into the blood, in periods of metabolic needs. These mechanisms are tightly regulated by hormonal and nervous signals, which are generated by specialized cells that detect variations in blood glucose or lipid concentrations. The hormones insulin and glucagon not only regulate glycemic levels through their action on these organs and the sympathetic and parasympathetic branches of the autonomic nervous system, which are activated by glucose or lipid sensors, but also modulate pancreatic hormone secretion and liver, muscle and fat glucose and lipid metabolism. Other signaling molecules, such as the adipocyte hormones leptin and adiponectin, have circulating plasma concentrations that reflect the level of fat stored in adipocytes. These signals are integrated at the level of the hypothalamus by the melanocortin pathway, which produces orexigenic and anorexigenic neuropeptides to control feeding behavior, energy expenditure and glucose homeostasis. Work from several laboratories, including ours, has explored the physiological role of glucose as a signal that regulates these homeostatic processes and has tested the hypothesis that the mechanism of glucose sensing that controls insulin secretion by the pancreatic beta-cells is also used by other cell types. I discuss here evidence for these mechanisms, how they integrate signals from other nutrients such as lipids and how their deregulation may initiate metabolic diseases.International Journal of Obesity (2008) 32, S62–S71; doi:10.1038/ijo.2008.208 [ABSTRACT FROM AUTHOR]

Although it is well established that the presence of nutrients in the gut lumen can bring about changes in GI function, the mechanisms and pathways by which these changes occur has not been fully elucidated. It has been known for many years that luminal nutrients stimulate the release of hormones and regulatory peptides from gut endocrine cells and that luminal nutrients activate intrinsic and extrinsic neural pathways innervating the gut. Activation of gut endocrine cells and neural pathways by nutrients in the gut lumen is key in coordination of postprandial GI function and also in the regulation of food intake. Recent evidence suggests that these pathways can be modified by long term changes in diet or by inflammatory processes in the gut wall. Thus it is important to determine the cellular and molecular mechanisms underlying these processes not only to increase our understanding of as part of basic physiology but also to understand changes in these pathways that occur in the presence of pathophysiology and disease. This review summarizes some of the latest data that we have obtained, together with information from the other laboratories, which have elucidated some of the mechanisms involved in nutrient detection in the gut wall. The focus is on monosaccharides and protein hydrolysates as there is some evidence for a role for nutrient transporters in detection of these nutrients. [ABSTRACT FROM AUTHOR]

The biosynthesis of the ketocarotenoid astaxanthin is a subject of scientific and industrial interest. The unicellular green alga Chlorella zofingiensis Dönz is able to grow and accumulate astaxanthin in the dark with exogenous glucose as sole carbon and energy source. In this study, the transcription of β-carotenoid ketolase (BKT) and β-carotenoid hydroxylase (CHYb) genes were surveyed to reveal the regulation of astaxanthin biosynthesis in dark-grown Chlorella zofingiensis. Coupled with glucose analogs and the hexokinase inhibitor glucosamine, we found that phosphorylation of glucose (glucose sensing) was essential to the increased transcription of BKT and CHYb genes and the accumulation of astaxanthin in the dark-grown cells. However, phosphorylation of glucose per se only up-regulated the transcription of CHYb and stimulated the synthesis of zeaxanthin. Blockage of the mitochondrial alternative pathway eliminated the glucose effects on the increased transcription of BKT and astaxanthin accumulation, suggesting that signals from alternative pathway was involved in the up-regulation of BKT transcription. In addition, citrate was shown to up-regulate the transcription of BKT independent of reactive oxygen species formation. Taken altogether, we conclude that in dark-grown Chlorella zofingiensis, the transcription of BKT and CHYb genes are differently regulated by the metabolism of glucose, through which the biosynthesis of astaxanthin is regulated . [ABSTRACT FROM AUTHOR]

Although cells expressing insulin are detected early in human fetal development, islets isolated from fetal pancreases show poor insulin secretory responses to glucose, which may be the result of deficient glucose sensing. We have used dual and triple immunolabelling of human fetal and adult pancreas sections to investigate the presence of proteins that participate in glucose sensing in the pancreatic beta cell, namely glucose transporter 1 (GLUT 1, also known as SLC2A1), glucose transporter 2 (GLUT2, also known as SLC2A2), glucokinase (GCK) and inwardly rectifying K+ channel (KIR6.2, also known as KCNJ11) and sulphonylurea receptor 1 (SUR1, also known as ABCC8) subunits of ATP-sensitive K+ channels ( $$ {\text{K}}^{ + }_{{{\text{ATP}}}} $$ channels). Pancreases obtained with ethical approval from human fetuses from 11 to 36 weeks of gestation, from infants and from adults were formalin-fixed and embedded in paraffin. Sections were labelled with antibodies to proteins of interest. Co-production of antigens was examined by dual and triple immunolabelling. GLUT2 and $$ {\text{K}}^{ + }_{{{\text{ATP}}}} $$ channel labelling was detected in the 11-week pancreas, but largely within the pancreatic epithelium, whereas no labelling for GLUT1 was observed. From 15 weeks, GLUT1, GCK and $$ {\text{K}}^{ + }_{{{\text{ATP}}}} $$ channel labelling was detected in an increasing proportion of insulin-positive cells and epithelial labelling with $$ {\text{K}}^{ + }_{{{\text{ATP}}}} $$ channel antibodies diminished. GLUT2 was seen in the majority of beta cells only after 7 months of age. The results demonstrate that only a subpopulation of beta cells in the human fetal pancreas produce all key elements of the glucose-sensing apparatus, which may contribute to poor secretory responses in early life. [ABSTRACT FROM AUTHOR]

The simultaneous use of several fluorescent reporter dyes in a multicomponent boronic acid-based glucose sensing system is reported. In one application, two dyes with widely different emission wavelengths are used to report changes in glucose concentration. A third glucose-insensitive dye was then added to act as a reference dye and provide for a ratiometric correction to the two reporter dye signals. The inclusion of such a reference dye reduces errors arising from sources such as fluctuations in lamp intensity and sample dilution. [Figure not available: see fulltext.] [ABSTRACT FROM AUTHOR]

The relation between plasma glucose and insulin release from pancreatic beta-cells is not stationary in the sense that a given glucose concentration leads to a specific rate of insulin secretion. A number of time-dependent mechanisms appear to exist that modify insulin release both on a short and a longer time scale. Typically, two phases are described. The first phase, lasting up to 10 min, is a pulse of insulin release in response to fast changes in glucose concentration. The second phase is a more steady increase of insulin release over minutes to hours, if the elevated glucose concentration is sustained. The paper describes the glucose sensing mechanism via the complex dynamics of the key enzyme glucokinase, which controls the first step in glucose metabolism: phosphorylation of glucose to glucose-6-phosphate. Three time-dependent phenomena (mechanisms) are described. The fastest, corresponding to the first phase, is a delayed negative feedback regulating the glucokinase activity. Due to the delay, a rapid glucose increase will cause a burst of activity in the glucose sensing system, before the glucokinase is down-regulated. The second mechanism corresponds to the translocation of glucokinase from an inactive to an active form. As the translocation is controlled by the product(s) of the glucokinase reaction rather than by the substrate glucose, this mechanism gives a positive, but saturable, feedback. Finally, the release of the insulin granules is assumed to be enhanced by previous glucose exposure, giving a so-called glucose memory to the beta-cells. The effect depends on the insulin release of the cells, and this mechanism constitutes a second positive, saturable feedback system. Taken together, the three phenomena describe most of the glucose sensing behaviour of the beta-cells. The results indicate that the insulin release is not a precise function of the plasma glucose concentration. It rather looks as if the beta-cells just increase the insulin production, until the plasma glucose has returned to normal. This type of integral control has the advantage that the precise glucose sensitivity of the beta-cells is not important for normal glucose homeostasis. [ABSTRACT FROM AUTHOR]

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Immobilization of bioactive molecules on the surface of magnetic nanoparticles is of great interest, because the magnetic properties of these bioconjugates promise to greatly improve the delivery and recovery of biomolecules in biomedical applications. Here we present the preparation and functionalization of magnetite (Fe3O4) nanoparticles 20 nm in diameter and the successful covalent conjugation of the enzyme glucose oxidase to the amino-modified nanoparticle surface. Functionalization of the magnetic nanoparticle surface with amino groups greatly increased the amount and activity of the immobilized enzyme compared with immobilization procedures involving physical adsorption. The enzymatic activity of the glucose oxidase-coated magnetic nanoparticles was investigated by monitoring oxygen consumption during the enzymatic oxidation of glucose using a ruthenium phenanthroline fluorescent complex for oxygen sensing. The glucose oxidase-coated magnetite nanoparticles could function as nanometric glucose sensors in glucose solutions of concentrations up to 20 mmol L-1. Immobilization of glucose oxidase on the nanoparticles also increased the stability of the enzyme. When stored at 4°C the nanoparticle suspensions maintained their bioactivity for up to 3 months. [ABSTRACT FROM AUTHOR]

A key aspect of glucose homeostasis is the constant monitoring of blood glucose concentrations by specific glucose sensing units. These sensors, via stimulation of hormone secretion and activation of the autonomic nervous system (ANS), regulate tissue glucose uptake, utilization or production. The best described glucose detection system is that of the pancreatic ß-cells which controls insulin secretion. Secretion of other hormones, in particular glucagon, and activation of the ANS, are regulated by glucose through sensing mechanisms which are much less well characterized. Here I review some of the studies we have performed over the recent years on a mouse model of impaired glucose sensing generated by inactivation of the gene for the glucose transporter GLUT2. This transporter catalyzes glucose uptake by pancreatic ß-cells, the first step in the signaling cascade leading to glucose-stimulated insulin secretion. Inactivation of its gene leads to a loss of glucose sensing and impaired insulin secretion. Transgenic reexpression of the transporter in GLUT2/β-cells restores their normal secretory function and rescues the mice from early death. As GLUT2 is also expressed in other tissues, these mice were then studied for the presence of other physiological defects due to absence of this transporter. These studies led to the identification of extra-pancreatic, GLUT2-dependent, glucose sensors controlling glucagon secretion and glucose utilization by peripheral tissues, in part through a control of the autonomic nervous system. [ABSTRACT FROM AUTHOR]

Autoimmune destruction of β cells in the pancreas leads to type I, or insulin dependent diabetes mellitus (IDDM), through the loss of endogenous insulin production capacity. This paper describes an attempt to generate ‘artificial’β cells using the fibroblast cell line BHK21. Stable transfectants expressing the human preproinsulin (PPI) gene were isolated and characterised. The resulting clone selected for further analysis (BHK-PPI-C16) was capable of secreting 0.12 pmol proinsulin/hr/105 cells and maintained a steady cellular proinsulin content of 0.36 ± 0.04 pmol l−1. There was no processing of the proinsulin to mature insulin. The cells were unresponsive to glucose but there was increased proinsulin secretion in the presence of agents that stimulated formation of intracellular cAMP. Transfection of cDNAs for the key elements of the glucose sensing apparatus (GLUT2 and glucokinase) led to a subphysiological stimulation of secretion when glucokinase was transfected alone while there was a complete loss of insulin secretion when both components were overexpressed. The deleterious effect on proinsulin secretion observed upon co-expression of the glucose sensing genes may have implications for applications requiring multigene expression in BHK21 cells. [ABSTRACT FROM AUTHOR]

Aims/hypothesis. The role of glucose sensing cells in the human hepatic portal system in the initiation of the neuroendocrine responses to acute hypoglycaemia is not known. We investigated the effect of raising blood glucose concentrations in the hepatic-portal vein on neurohumoral responses during induction of systemic hypoglycaemia in nine healthy male volunteers. Methods. Each subject received an insulin infusion (3 mU·kg–1·min–1) on two occasions, in random order. Variable rate glucose infusion was used to maintain plasma glucose at 5 mmol/l for 60 min, then 3.2 mmol/l for 60 min. At 20 min prior to hypoglycaemia, subjects drank 20 g of glucose in water or water sweetened with saccharin. In five of the volunteers, the oral glucose was labelled with U-13C6 glucose, which showed peak systemic glucose absorption between 90 and 110 min. Five volunteers also repeated the study with a euglycaemic clamp. Results. Oral glucose was associated with a reduction in the early adrenaline response to hypoglycaemia, the area under the curve from 90 to 110 min falling from 24.02±20.84 (means ± SD) to 15.26±13.65 nmol/l per 20 min, p<0.05. Symptom scores (area under curve) decreased from 99.72±91.86 to 16.39±94.71, p=0.008 (total), 51.8±68.61 to 7.78±41.61, p=0.03 (autonomic) and 54.17±50.61 to 8.6±57.99 with oral glucose, p=0.001 (neuroglycopenic). Oral glucose did not influence symptoms during euglycaemia. Conclusion/Interpretation. Our data are compatible with the hypothesis that centrally mediated symptomatic and neuroendocrine responses are attenuated by glucose detection in the hepatic portal vein in humans. [ABSTRACT FROM AUTHOR]

Aims. Within the brain, subgroups of neurons respond differently to altered glucose concentrations. Identification of neuropeptide Y in hypothalamic neurons that sense glucose suggests a role for neuropeptide Y in glucose sensing. Using in vitro and in vivo techniques to monitor transmitter release, we investigated whether lowering glucose concentration affects the release of neuropeptide Y from the brain, and whether this process is altered in Type I (insulin-dependent) diabetes mellitus. Methods. Male Sprague-Dawley rats were treated with 48 mg/kg streptozotocin or vehicle intravenously. The effect of reduced glucose on endogenous neuropeptide Y overflow from slices of hypothalamus and medulla incubated in Krebs solution was examined 4 weeks later. The hypothalamus was separated into a dorsal region containing the paraventricular nucleus and a ventral region containing the arcuate nucleus. Results.Streptozotocin-induced diabetes increased basal neuropeptide Y overflow in the dorsal and ventral hypothalamus (p<0.05) but not the medulla. In vitro neuropeptide Y overflow was reduced by low glucose in the dorsal hypothalamus in diabetic, but not in control rats. No effect of reduced glucose was observed in the ventral hypothalamus or medulla. In vivo push-pull studies in the paraventricular nucleus also showed greater neuropeptide Y overflow in diabetic rats relative to control rats (p<0.05). Insulin-induced hypoglycaemia induced a decrease in neuropeptide Y overflow in diabetic rats, while an increase was observed in control rats (p<0.05). Conclusion. These region-specific effects of low glucose on neuropeptide Y overflow in diabetic rats support a part for neuropeptide Y in altered glucose sensing in Type I diabetes. [ABSTRACT FROM AUTHOR]