Effects of GLP-1 and Its Analogs on Gastric Physiology in Diabetes and Obesity
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This initiates a cascade that leads to the activation of protein kinase A (PKA), closing of potassium channels, depolarization, and release of calcium from the endoplasmic reticulum.3 An increase of intracellular calcium levels within the cell initiates insulin expression in the nucleus, stimulates energy (ATP) production in the mitochondria, and triggers the release of insulin into the blood stream in a glucose dependent manner (image adapted from Adipogen Life Sciences).4,5 Several commercially and prescribed agents are now available for the management of obesity and type 2 diabetes
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