The new finding reveals a novel function of LDL as a regulator of fat turnover, besides its well-established detrimental effects in promoting atherosclerosis.
During the study, the researchers found that LDL cholesterol slows the rate of fat breakdown (i.e. lipolysis) in adipocytes, the peripheral cells responsible for fat storage.
Previous studies have shown the fatty acids released from the peripheral fat to the blood boost the synthesis of LDL precursors in the liver.
"The results of our study provide evidence of a reciprocal link between the liver and peripheral fat regulating fat turnover", said study-initiator Dr Johan Bjorkegren.
The finding also opens up for new theories for the well-established association between blood lipids and the metabolic syndrome.
"If proven of general physiological importance, therapies lowering LDL, as for instances Statins, may also affect the turnover of peripheral fat," Bjorkegren said.
The study was conducted on cell cultures and tissues from humans as well as mouse models with different levels of LDL.
The inhibitory effect was also shown to be dependent on LDL receptors on the surface of the fat cells.
Project leader Dr Josefin Skogsberg said: "The exact intracellular mechanism for how the binding of LDL to the surface of the fat cells inhibits the breakdown of intracellular fat remains to be revealed."
The study is published in the open-access journal PLoS ONE.