What is the mechanism of action of Niacin (Nicotinic acid) versus Fibrates in decreasing serum Triglycerides?

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From the Guidelines

Niacin and fibrates are both effective in reducing serum triglycerides, but fibrates are generally more potent, with a triglyceride reduction of 30-50% compared to niacin's 20-50% reduction, as shown in a study published in Circulation 1. The mechanism of action of niacin and fibrates differs, with niacin primarily decreasing triglycerides by inhibiting the enzyme diacylglycerol acyltransferase-2 (DGAT-2) in the liver and suppressing lipolysis in adipose tissue by binding to the GPR109A receptor.

  • Niacin's effects on triglyceride reduction are dose-dependent, with therapeutic doses of 1-2 grams daily typically reducing triglycerides by 20-50%.
  • Fibrates, such as fenofibrate and gemfibrozil, work primarily as peroxisome proliferator-activated receptor alpha (PPAR-α) agonists, increasing the expression of lipoprotein lipase and enhancing triglyceride clearance from the bloodstream.
  • Fibrates also increase fatty acid oxidation in the liver and reduce the synthesis of apolipoprotein C-III, which normally inhibits lipoprotein lipase, as noted in guidelines published in the American Family Physician 1. The choice between niacin and fibrates for reducing serum triglycerides should be based on individual patient factors, including the presence of other cardiovascular risk factors and the potential for side effects, such as flushing with niacin.
  • Fibrates are generally better tolerated than niacin and may be preferred in patients with severe hypertriglyceridemia or those at risk of pancreatitis.
  • However, niacin may be a suitable alternative for patients who cannot tolerate fibrates or require additional lipid-lowering therapy, as suggested by guidelines published in the American Family Physician 1.

From the FDA Drug Label

The active moiety of fenofibrate tablet is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively studied through oral administration of fenofibrate The lipid-modifying effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα) Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity) The mechanism by which niacin alters lipid profiles has not been well defined. It may involve several actions including partial inhibition of release of free fatty acids from adipose tissue, and increased lipoprotein lipase activity, which may increase the rate of chylomicron triglyceride removal from plasma Niacin decreases the rate of hepatic synthesis of VLDL and LDL, and does not appear to affect fecal excretion of fats, sterols, or bile acids.

The mechanism of action of fenofibrate in decreasing serum triglycerides involves the activation of peroxisome proliferator activated receptor α (PPARα), which increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III. In contrast, the mechanism of action of niacin is not well defined, but may involve partial inhibition of release of free fatty acids from adipose tissue, increased lipoprotein lipase activity, and decreased hepatic synthesis of VLDL and LDL 2 3. Key differences between the two mechanisms include:

  • Receptor activation: Fenofibrate activates PPARα, while niacin's mechanism does not involve a specific receptor.
  • Lipid metabolism: Fenofibrate increases lipolysis and elimination of triglyceride-rich particles, while niacin decreases hepatic synthesis of VLDL and LDL.

From the Research

Mechanism of Action of Niacin and Fibrates

The mechanism of action of niacin and fibrates in decreasing serum triglycerides involves several key aspects:

  • Niacin and fibrates are lipid-lowering drugs that raise high-density lipoprotein cholesterol (HDL-C), reduce triglycerides and non-HDL-C, but have a modest effect on reducing low-density lipoprotein cholesterol (LDL-C) 4.
  • Fibrates primarily target the reduction of triglyceride-rich lipoproteins and remnant particles, which contributes to the reduction of residual cardiovascular disease (CVD) risk 5.
  • Niacin, on the other hand, is the most potent HDL-increasing drug currently available and also efficaciously lowers triglycerides and LDL cholesterol 6.

Comparison of Niacin and Fibrates

Key differences between niacin and fibrates include:

  • Fibrates may continue to have a role in the treatment of extreme hypertriglyceridemia and in mixed hyperlipidaemia, as they reduce CVD events and have additional benefits in improving diabetes and microvascular outcomes 4.
  • Niacin, however, may have little role in the treatment of hyperlipidaemia, with other options in development to lower LDL-C further, raise HDL-C, or reduce lipoprotein(a) potentially replacing niacin 4.
  • Both niacin and fibrates have been shown to be effective as adjunctive therapy for low HDL and high triglycerides, but their use is often below expectations based on guideline recommendations 7.

Clinical Implications

The clinical implications of using niacin and fibrates to decrease serum triglycerides include:

  • Guidelines recommend the addition of fibrates, niacin, or long-chain omega-3 fatty acids if elevated triglyceride or non-high-density lipoprotein cholesterol levels persist despite the use of high-intensity statin therapy 5.
  • Outcome studies with triglyceride-lowering agents have been inconsistent, but subgroup analyses suggest that triglyceride lowering may provide benefit in statin-treated patients with persistent hypertriglyceridemia 8.
  • Ongoing studies, such as the REDUCE-IT and STRENGTH trials, are testing the hypothesis that triglyceride lowering with omega-3 fatty acids can improve atherosclerotic cardiovascular disease outcomes in high-risk, statin-treated patients with triglyceride levels of 200 to 500 mg/dL 8.

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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