Fenofibrate lowers triglycerides primarily through activation of which receptor?

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Multiple Choice

Fenofibrate lowers triglycerides primarily through activation of which receptor?

Fenofibrate lowers triglycerides mainly by activating a nuclear receptor in the liver called PPARα. When PPARα is activated, it upregulates genes involved in fatty acid oxidation and increases the activity of lipoprotein lipase, which enhances the clearance of triglyceride-rich particles and reduces hepatic production of VLDL. The result is a substantial drop in plasma triglycerides, with a modest rise in HDL. Other receptors listed have different primary roles that don’t drive the triglyceride-lowering effect of fenofibrate. PPARγ is mainly about adipocyte function and insulin sensitivity; LXR influences cholesterol metabolism and lipogenesis; FXR governs bile acid synthesis and overall hepatic lipid handling, but not the main mechanism behind fenofibrate’s triglyceride reduction.

Fenofibrate lowers triglycerides mainly by activating a nuclear receptor in the liver called PPARα. When PPARα is activated, it upregulates genes involved in fatty acid oxidation and increases the activity of lipoprotein lipase, which enhances the clearance of triglyceride-rich particles and reduces hepatic production of VLDL. The result is a substantial drop in plasma triglycerides, with a modest rise in HDL.

Other receptors listed have different primary roles that don’t drive the triglyceride-lowering effect of fenofibrate. PPARγ is mainly about adipocyte function and insulin sensitivity; LXR influences cholesterol metabolism and lipogenesis; FXR governs bile acid synthesis and overall hepatic lipid handling, but not the main mechanism behind fenofibrate’s triglyceride reduction.

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