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Fibrates stimulate the PPAR-alpha receptors. This leads to increased lipoprotein lipase activity. More triglycerides get broken down into free fatty acids which get reuptaken or beta-oxidised. As there are less triglycerides, less LDL and VLDL is produced. Due to increased ApoA-I, the production of HDL also increases.

Niacin inhibits the niacin receptor. This leads to the inhibition of cAMP production and PKA activity. This therefore inhibits the activity of hormone-sensitive lipase. Fewer triglycerides get broken down into free fatty acids. As the free fatty acid level in plasma is lower, the hepatic synthesis of VLDL decreases. Less VLDL also results in less conversion into LDL. Niacin's effect on lowering triglycerides is not as obvious as fibrates. Niacin can also increase the amount of HDL as it can prolong the half-life of ApoA-I, leading to a greater bioavailability of ApoA-I for producing HDL.

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Q: How are the mechanisms of action of fibrates and niacin in treating dyslipidaemia different?
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