Glucose Insulin Treatment
Glucose Insulin Treatment - Related Videos
04:41
Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas
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2025
Here, we provide details on performing glucose-stimulated insulin secretion (GSIS) via perfusion through the mice vasculature with an intact pancreas as an additional technique to assess the endocrine pancreatic function with reduction of possible confounders.
08:03
Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
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Cited by 14 •
2017
In this method, human primary muscle cells are cultured in vitro to obtain differentiated myotubes and glucose uptake rates are measured. We provide a detailed protocol to quantify rates in basal and insulin-stimulated states using radiolabeled [3H] 2-deoxy-D-Glucose.
05:52
In Vitro Glucose Depletion Assay: A Fluorescence-Based Method to Quantify Cellular Glucose Uptake via Extracellular Glucose Depletion Measurement
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2025
This video demonstrates an in vitro assay to indirectly measure intracellular glucose uptake. The assay uses a fluorescently-labeled glucose analog to establish a correlation between extracellular glucose depletion and intracellular glucose uptake.
01:27
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
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2024
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell. Insulin and C-peptide are co-secreted in...
02:33
Assessing Atmospheric Pressure Plasma Treatment in Glucose-Deprived Neuroblastoma Cells
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2025
Source: Yan, X., et. al., New Application of an Atmospheric Pressure Plasma Jet as a Neuro-protective Agent Against Glucose Deprivation-induced Injury of SH-SY5Y Cells. J. Vis. Exp. (2017)The video demonstrates the neuroprotective activity of low-dose atmospheric pressure plasma treatment in glucose-deprived neuroblastoma cells by modulating oxidative stress and enhancing cell viability.
FAQs
Insulin begins its metabolic effect by binding to receptors on the cell surface. The resulting signaling increases glucose uptake in muscle and adipose cells, while also reducing glucose production by the liver. These coordinated actions help shift glucose from circulation into tissues and limit continued hepatic release, supporting more stable blood glucose control.
These tissues contribute to blood glucose balance in different ways. Muscle and adipose cells remove glucose from the circulation when insulin signaling promotes uptake, whereas the liver is a major source of glucose production that insulin suppresses. Addressing both uptake and production is therefore important for maintaining metabolic stability rather than influencing only one side of glucose regulation.
Dosing determines the strength of the intended glucose-lowering effect, while monitoring shows whether that effect is producing an appropriate metabolic response. Their combination helps identify the need to avoid both hypoglycemia and hyperglycemia. Controlled glucose administration may also be incorporated, allowing glucose availability and insulin action to be managed together when metabolic stability requires it.
Infection and inflammation can disrupt glucose control, making metabolic status an important part of care and investigation. In this setting, glucose-insulin management is not separate from host defense: altered glucose regulation may accompany infectious disease, while metabolic conditions can influence immune responses and recovery. Monitoring this interaction helps frame treatment within the broader physiology of illness.
Application centers on selecting an insulin dose, deciding whether controlled glucose administration is needed, and monitoring blood glucose during management. The purpose is to maintain metabolic stability while limiting excursions toward hypo- or hyperglycemia. In infection-related settings, these decisions are considered alongside the disruption of glucose control that may accompany infection and inflammation.
It becomes particularly relevant when infection or inflammation is associated with disturbed glucose regulation. The approach provides a way to study or manage metabolic stability while examining how altered metabolism relates to host defense and recovery. Its value in immunology and infection therefore extends beyond glucose measurement alone, linking therapeutic management with the biology of infectious disease.
Researchers can examine whether glucose levels remain within a stable range, whether treatment avoids hypo- and hyperglycemia, and how metabolic status relates to immune responses or recovery. These observations help connect insulin action and glucose control with infectious-disease biology. They also support investigation of how metabolic management may affect the interaction between host defense and illness-related physiological changes.