STOCKHOLM, Sweden—LDL inhibits the breakdown of fat in cells of peripheral deposits, said a study from Karolinska Institutet. The discovery reveals a novel function of LDL as a regulator of fat turnover in addition to its well-established detrimental effects in promoting atherosclerosis.
The study showed LDL cholesterol slows the rate of fat breakdown in adipocytes, the peripheral cells responsible for fat storage. Previously, it has been known that release of free fatty acid from the peripheral fat to the blood stream increases the synthesis of LDL precursors in the liver. The collaborative study by two research groups at Karolinska Institutet was published in the journal PLoS ONE.
“The results of our study provide evidence of a reciprocal link between the liver and peripheral fat regulating fat turnover,” said study-initiator Johan Björkegren, MD.
The discovery also opens up new theories for the well-established association between blood lipids and the metabolic syndrome.
The study has been performed on cell cultures and tissues from humans, as well as mouse models, with different levels of LDL. The inhibitory effect also was shown to be dependent on LDL receptors on the surface of the fat cells.
“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,” said project leader Josefin Skogsberg, MD.
