China
Africa
Explore chapters and articles related to this topic
Nanosensor Arrays
Published in Suresh Kaushik, Vijay Soni, Efstathia Skotti, Nanosensors for Futuristic Smart and Intelligent Healthcare Systems, 2022
Naumih M. Noah, Peter M. Ndangili
Urine as an analyte has been used for noninvasive detection of glucose since when the renal threshold for glucose is exceeded (for most individuals ~ 10 millimole/liter (mmol/L), it starts to be secreted with urine (Leroux 2001). Normally, glucose and other components are present in urine in very small quantities and glucose overflows into the urine when the blood glucose level is high, causing urine to have a sweet or fruity odor (Su et al. 2012). The existence of high levels of glucose in urine (more than 50–100 mg/dL) is considered a dangerous condition since it indicates the worsening of diabetes (Su et al. 2012). Several nanosensors for the detection of glucose in urine have been developed as alternatives to commercial low-cost colorimetric dipsticks including a reusable and stable nanosensor composed of a composite of gold-graphene oxide electrodes (Kim et al. 2014). The use of ZnFe2O4 magnetic nanoparticles has also been utilized in the development of a simple, inexpensive, highly sensitive, and selective colorimetric nanobiosensor for the detection of urine glucose using glucose oxidase (GOX) with a linear detection range of between 1.25 × 10–6 to 1.875 × 10–5 mol L–1 with a detection limit of 3.0 × 10–7 mol L–1 (Su et al. 2012). These characteristics of the nanobiosensors were attributed to the high catalytic efficiency, good stability, monodispersion, and rapid separation of the zinc-iron oxide ZnFe2O4 magnetic nanoparticles (MNPs) (Su et al. 2012).
Diabetes Mellitus/Anti-DM Pharmacological Management
Published in Mihai V. Putz, New Frontiers in Nanochemistry, 2020
Bogdan Bumbăcilă, Corina Duda-Seiman, Daniel Duda-Seiman, Mihai V. Putz
Glucosuria, the presence of glucose in the urine, has long been regarded as a consequence of uncontrolled diabetes. However, glucose excretion can be induced by blocking the activity of the renal sodium-glucose cotransporter 2 (SGLT-2). This mechanism corrects hyperglycemia independently of insulin, because SGLT2 is the major cotransporter involved in glucose reabsorption in the kidney. By lowering the renal threshold for glucose excretion, SGLT-2 inhibitors suppress renal glucose reabsorption (30–50% of the glucose filtered by the kidney) and thereby increase urinary glucose excretion. The advantages of this approach are reduced hyperglycemia without hypoglycemia, along with weight loss and blood pressure reduction (Chao, 2014).
Backstepping Model Predictive Controller for Blood Glucose Regulation in Type-I Diabetes Patient
Published in IETE Journal of Research, 2020
Akshaya Kumar Patra, Alok Kumar Mishra, Pravat Kumar Rout
The -cells of the pancreas are responsible for the insulin creation and this amount regulates the BG level. Majorly, the insulin functions in two ways in the normal human body operation. Firstly, under high BG level, particularly under meal intake, it allows the liver to absorb the glucose and store as glycogen. This in turn shuts off excess “internal” glucose production in the liver and muscles. Secondly, insulin operates as a catalyst to promote glucose absorption in the muscles and periphery for energy need [20,21]. But due to some abnormality in the dynamics of the metabolic process, both the above functions are partially or fully reduced in case of diabetes patients. BG level leads to an uncontrolled stage as cells stop to utilize the glucose and liver produces the internal glucose. Later, under the condition of a BG level exceeds the renal threshold glucose (RTG) value of 162 mg/dl, the extra glucose present in the venous blood is released through urine.