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Production Assistant, Diabetes In Control

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #32: Beta-Cell biology of insulin secretion Part 2 of 5

Metabolism-secretion coupling, triggering pathway: Glucose metabolism increases the cytosolic ATP concentration in pancreatic beta cells, this rise in ATP causing closure of the KATP channels and depolarization of the beta-cell membrane. Thus, KATP channels couple the cell’s metabolic state to electrical activity. The beta-cell KATP channel is composed of two subunits: Kir6.2 as a pore-forming subunit and the sulfonylurea receptor SUR1 as a regulatory subunit. Activity of the KATP channel is critical for GIIS. Membrane depolarization opens VDCCs, which allows Ca2+ influx into β cells, the resultant rise in intracellular Ca2+ triggering exocytosis of insulin granules. Thus, KATP channels and VDCCs are major ion channels required for metabolism-secretion coupling in insulin release.

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Bariatric Surgery Recommendations

Are you changing your criteria for recommending metabolic surgery to your patients based on the new guidelines issued by International Diabetes Federation Taskforce on Epidemiology and Prevention of Diabetes (see article 1)?

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #31: Beta-Cell Biology of Insulin Secretion Part 1 of 5

In pancreatic beta cells, glucose metabolism is essential for the regulation of insulin secretion. Glucose is taken up by glucose transporters and metabolized to generate adenosine triphosphate (ATP), which is the main driver of glucose-induced insulin secretion (GIIS). Increased cytosolic ATP causes closure of ATP-sensitive K+ (KATP) channels, depolarizing the plasma membrane, leading to the opening of voltage-dependent Ca2+ channels (VDCCs), which allows Ca2+ influx. The resultant rise in intracellular Ca2+ concentration ([Ca2+]i) induces exocytosis of insulin granules in the triggering pathway of insulin secretion. In addition, other signals generated by glucose amplify insulin secretion. Lipid metabolism is also involved in GIIS by interacting with glucose metabolism.

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