Researchers Discover A New Player In Lipid Metabolism
Mice lacking a particular gene did not gain weight when they were fed a typical high-fat, obesity-inducing Western diet, according to a new study. These mice were given the same amount of diet as their normal counterparts that gained weight.
Researchers engineered the mice with fat cells that lacked gene named SEL1L. The gene is also known to be involved in the clearance of misfolded proteins in the cell's protein making machinery called the endoplasmic recticulum.
"The million-dollar question is why don't these mice gain weight? Is this related to its inability to clear misfolded proteins in the ER?" said Ling Qi, associate professor of molecular and biochemical nutrition and senior author of the study, in the press release.
However, during the study, experimental mice developed a host of other problems as well. The problems included postprandial hypertriglyceridemia, which is characterized by high levels of triglycerides in humans and mice (after a meal) that can lead to heart attacks and strokes if untreated, and fatty livers.
"Although we are yet to find out whether these conditions contribute to the lean phenotype, we found that there was a lipid partitioning defect in the mice lacking SEL1L in fat cells, where fat cells cannot store fat [lipids], and consequently fat goes to the liver. During the investigation of possible underlying mechanisms, we discovered a novel function for SEL1L as a regulator of lipid metabolism," said Qi.
"We were very excited to find that SEL1L is required for the intracellular trafficking of an enzyme called lipoprotein lipase (LPL), acting as a chaperone. Using several tissue-specific knockout mouse models, we showed that this is a general phenomenon," added lead author Haibo Sha, a research associate in Qi's lab.
The study has been published in the journal Cell Metabolism.