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A research team has uncovered the likely target of niacin (vitamin
B3) in the liver, which should provide a clearer picture of how this
vitamin helps maintain adequate HDL-cholesterol levels in the blood and
thus lower the risk of heart disease. While niacin can increase plasma
HDL levels, the mechanism of how it works has been mysterious, although
it's believed that niacin does not actually increase HDL production.
Recent work had uncovered that a component of ATP synthase (the protein
that makes ATP) is present on the surface of liver cells, and this
subunit known as the 'beta chain' can take up HDL.
Now, Moti Kashyap and colleagues found that this beta chain is the
basis of niacin's effect. They added niacin to samples of human liver
cells and found that treatment reduced the presence of Beta chain on
the cell surface by ~27%, and as a result HDL uptake was reduced by
~35%. In comparison, nicotinamide, a related molecule with no clinical
benefit, had far weaker effects.
These results indicate niacin hinders the liver from removing HDL
from the blood, thus maintaining high plasma HDL levels. Importantly,
niacin does not affect another major pathway known as "Reverse
Cholesterol Transport." Therefore, it maintains HDL levels while still
allowing the removal of other cholesterol types, explaining why niacin
is especially beneficial.
The work also identifies a new drug target, as no other drug in
currently known to raise HDL by inhibiting the surface expression of
the beta chain of ATP synthase.
Source: American Society for Biochemistry and Molecular Biology .
Article abstract: Zhang, L. H., Kamanna, V. S.,
Zhang, M. C. and
Moti L. Kashyap, M. L.. Niacin inhibits surface expression of ATP synthase B-chain in HepG2 cells: implications for raising HDL.
Journal of Lipid Research, Vol. 49, 1195-1201, June 2008.
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