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- Assay Type Detection Kit
- Sample Types Serum, Plasma, Urine, Buffers, Tissue Culture Media
- Sensitivity 0.413 mg/dL
- Species Species Independent
- Assay Duration 30 Minutes
- Samples/Plate 40 in duplicate
- Readout Colorimetric, 560 nm
- Standard Curve
The Glucose Colorimetric Detection Kit quantitatively measures Glucose levels in serum, plasma, urine, buffers, and tissue culture media. The Glucose Colorimetric Detection Kit is a Detection Kit with a run time of 30 minutes. Please read the complete kit insert for more information before performing this assay.
Use our provided Glucose standard to generate a standard curve for the assay. Pipette the standards or diluted samples into a clear microtiter plate. Add Substrate, Horseradish Peroxidase Concentrate, and Glucose Oxidase Concentrate to each well, tapping the plate to ensure sufficient mixing of reagents. Then, incubate the mixture at room temperature for 30 minutes. The glucose oxidase reacts with glucose to produce hydrogen peroxide, which, in the presence of HRP, reacts with the substrate to generate a pink-colored product.
After the 30-minute incubation, use a plate reader to detect and record the generated signal at 560nm. Use the intensity and the standard curve to calculate the Glucose concentration in the samples.
Glucose is by far the most common carbohydrate energy source for the cell. It is a monosaccharide, an aldose, a hexose, and a reducing sugar. It is also known as dextrose because it is dextrorotatory (rotates polarized light clockwise). Energy is essential for all biological and molecular events and multiple cellular functions. Reduced energy levels threaten cellular homeostasis and integrity. Impaired energy metabolism may trigger pro-apoptotic signaling (programmed cell death), oxidative damage, excitotoxicity, and impede mitochondrial DNA repair.
A severe drop in blood glucose can be characterized by metabolic dysfunction, neuroglycopenia, seizure, and death. A persistent elevation in blood glucose leads to “glucose toxicity.” Glucose toxicity contributes to β-cell dysfunction and the pathology grouped as complications of diabetes. Estrogen-induced signaling pathways in hippocampal and cortical neurons involve the mitochondria to enhance mitochondrial function and to sustain aerobic glycolysis and citric acid cycle oxidative phosphorylation and ATP generation.