Which class of drugs reduces insulin resistance?

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Multiple Choice

Which class of drugs reduces insulin resistance?

Explanation:
Insulin resistance is addressed by drugs that make the body's tissues respond better to insulin rather than increasing how much insulin is produced. Thiazolidinediones do exactly that. They activate PPAR gamma in adipose tissue (and to some extent in muscle), which reprograms gene expression to favor healthier fat storage and improve insulin signaling. This leads to more glucose being taken up by muscle and fat cells and reduces the liver’s tendency to produce glucose, all of which lowers insulin resistance over time. They also raise adiponectin levels, which further enhances insulin sensitivity. In contrast, the other classes work differently. Sulfonylureas stimulate the pancreas to release more insulin, addressing insulin secretion rather than sensitivity. Meglitinides work similarly by boosting insulin release in response to meals. SGLT2 inhibitors lower blood glucose by causing the kidneys to dump glucose in the urine, an insulin-independent mechanism that doesn’t directly improve how tissues respond to insulin.

Insulin resistance is addressed by drugs that make the body's tissues respond better to insulin rather than increasing how much insulin is produced. Thiazolidinediones do exactly that. They activate PPAR gamma in adipose tissue (and to some extent in muscle), which reprograms gene expression to favor healthier fat storage and improve insulin signaling. This leads to more glucose being taken up by muscle and fat cells and reduces the liver’s tendency to produce glucose, all of which lowers insulin resistance over time. They also raise adiponectin levels, which further enhances insulin sensitivity.

In contrast, the other classes work differently. Sulfonylureas stimulate the pancreas to release more insulin, addressing insulin secretion rather than sensitivity. Meglitinides work similarly by boosting insulin release in response to meals. SGLT2 inhibitors lower blood glucose by causing the kidneys to dump glucose in the urine, an insulin-independent mechanism that doesn’t directly improve how tissues respond to insulin.

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