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Niacin’s mechanism of action has been determined, revealing a new drug target

Wednesday, January 28th, 2009

Source: Zhang LH, Kamanna VS, Zhang MC, Kashyap ML: Niacin inhibits surface expression of ATP synthase β-chain in HepG2 cells: implications for raisingHDL.
J. Lipid Res. 49(6), 1195-1201 (2008).

Niacin, also known as vitamin B3, can lower blood lipid levels. It may be used in the treatment of hyperlipidemia, where it reduces the LDL precursor VLDL. Niacin locks the breakdown of fats, resulting in a decrease in blood free fatty acid levels and consequently decreased VLDL and cholesterol secretion by the liver. In addition, by
lowering VLDL levels niacin also increases HDL levels.

Until recently, the mechanism of action of niacin was unknown, although it was thought that it did not increase HDL production. However, Moti Kashyap and colleagues (Veterans Administration Healthcare System, CA, USA) have now identified the ATP synthase β-chain as the likely target of niacin. This finding provides a clearer picture of how niacin maintains adequate blood HDL-C levels, thereby lowering the risk of heart disease.

Recently, it was shown that a component of ATP synthase is present on the surface of liver cells. This component was identified as the β-chain, which was found to be a HDL/ApoA-I receptor for HDL endocytosis in liver cells. Kashyap and colleagues demonstrated that niacin exerts its effects through this β-chain. Niacin was added to human HepG2 cells, leading to a 27% decrease in β-chain cell surface expression.

As a result, HDL uptake was reduced to 35%. By comparison, nicotinamide, a niacin metabolite that does not have a clinical effect on lipid levels, had weaker effects. HDL uptake was also reduced by the addition of anti-β-chain antibody; moreover, addition of the antibody abolished the inhibitory effect of niacin. β-chain mRNA expression was not altered by niacin administration.

The results from this study suggest that niacin reduces the liver’s capacity to remove HDL from the blood by a mechanism that inhibits the cell surface expression of ATP synthase β-chain. As a result, this maintains high HDL plasma levels. It should be noted that niacin does not affect the reverse cholesterol transport pathway. This is important as it means that HDL levels can be maintained, but other cholesterol types can still be removed from the blood.

The ATP synthase β-chain may be a new drug target, as no other drug is currently known to raise HDL levels by the reported mechanism.

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Tags: cholesterol, endur-acin, Enduracin, HDL-C levels, lipid levels, niacin, synthase β-chain, vldl
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