Sulfonylurea MOA?

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Multiple Choice

Sulfonylurea MOA?

Explanation:
Sulfonylureas promote insulin release from pancreatic beta cells by closing the ATP-sensitive potassium (KATP) channels. When these channels close, the beta-cell membrane depolarizes, voltage-gated calcium channels open, calcium rushes into the cell, and insulin-containing granules are released. This mechanism relies on functional beta cells to secrete insulin, which is why these drugs are effective in type 2 diabetes with preserved beta-cell function but not in absolute insulin deficiency. They do not primarily reduce hepatic glucose production, nor do they decrease glucose absorption from the gut or increase insulin sensitivity in muscle—that’s the actions of metformin, alpha-glucosidase inhibitors, and thiazolidinediones, respectively.

Sulfonylureas promote insulin release from pancreatic beta cells by closing the ATP-sensitive potassium (KATP) channels. When these channels close, the beta-cell membrane depolarizes, voltage-gated calcium channels open, calcium rushes into the cell, and insulin-containing granules are released. This mechanism relies on functional beta cells to secrete insulin, which is why these drugs are effective in type 2 diabetes with preserved beta-cell function but not in absolute insulin deficiency. They do not primarily reduce hepatic glucose production, nor do they decrease glucose absorption from the gut or increase insulin sensitivity in muscle—that’s the actions of metformin, alpha-glucosidase inhibitors, and thiazolidinediones, respectively.

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