Insulin Stimulation
Insulin Stimulation - 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
Insulin Injection and Hemolymph Extraction to Measure Insulin Sensitivity in Adult Drosophila melanogaster
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Cited by 16 •
2011
Conserved insulin signaling pathways found in the fruit fly Drosophila melanogaster make this organism a potential tool for modeling metabolic disorders including type II diabetes. To this end, it is critical to establish physiological assays to effectively measure systemic insulin action in peripheral glucose disposal in the adult fly.
14:39
A Quantitative Assay for Insulin-expressing Colony-forming Progenitors
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Cited by 11 •
2011
A three-dimensional clonogenic assay that allows pancreatic-like progenitors to differentiate into insulin-expressing colonies is described. This method takes advantage of semi-solid media containing methylcellulose, Matrigel and growth factors, in which single progenitors proliferate and differentiate in vitro, permitting quantification of the number of functional progenitors in a population.
12:08
Improving IV Insulin Administration in a Community Hospital
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Cited by 7 •
2012
When compared to the previous paper protocol, implementation of a computerized glucose management system results in a substantial increase in blood glucose concentration measurements within the target range. Using a computerized glucose management system to monitor blood glucose levels, decreases in severe hypoglycemia (<40 mg/dL), clinical hypoglycemia (<70 mg/dL), and hyperglycemia (>180 mg/dL) also can be observed.
FAQs
ATP-sensitive potassium channels provide the electrical link between glucose metabolism and beta-cell secretion. When glucose metabolism raises intracellular ATP, these channels close, reducing potassium movement across the membrane. The resulting depolarization activates voltage-gated calcium channels, creating the signal needed for insulin-containing granules to move toward membrane fusion. This sequence connects nutrient sensing with secretion.
Calcium influx acts as the immediate trigger for insulin-containing granules to fuse with the beta-cell membrane. Membrane depolarization opens voltage-gated calcium channels, allowing calcium to enter after ATP-sensitive potassium channels close. Without this calcium-dependent step, the metabolic signal generated by glucose would not be efficiently converted into release of stored insulin.
Nutrients, hormones, and experimental compounds can influence insulin secretion or insulin activity through metabolic signaling in beta cells. Their effects may be studied by examining how each signal changes the response associated with glucose metabolism, membrane electrical state, calcium entry, or granule release. This comparison helps identify which signals enhance or modify beta-cell function.
An investigation can expose beta-cell systems to a selected nutrient, hormone, or compound and assess the resulting change in insulin secretion or activity. Interpreting the response alongside the glucose-to-calcium signaling sequence helps distinguish effects on metabolism, membrane depolarization, calcium entry, or granule fusion. Such experiments support systematic analysis of metabolic signaling.
Insulin stimulation provides a way to evaluate how candidate compounds affect insulin secretion or activity in relation to glucose-regulated signaling. Compounds can be compared according to whether they alter beta-cell responses or influence pathways connected with nutrient use. This application supports diabetes research by identifying substances that may modify impaired metabolic regulation.
The process links beta-cell activity with the regulation of blood glucose and cellular nutrient use, making it central to glucose homeostasis. Studying the response can reveal how effectively beta cells translate metabolic signals into insulin release or activity. These findings provide biological context for insulin resistance and for experiments investigating diabetes-related changes in metabolic signaling.