Subjects: R and D
Scientists at UC Berkeley have found that mice with a genetically engineered defect in a fat tissue enzyme remained thin despite gorging to their heart’s content on a high-fat diet.
The enzyme is adipose-specific phospholipase A2 or AdPLA. It normally catalyzes a biochemical process that produces prostaglandin E2. High PGE2 levels suppress fat metabolism. The AdPLA-deficient mice had low PGE2 levels and broke down fat like crazy.
Kathy Jaworski and her colleagues bred mice that produced an inactive form of AdPLA and offered them and a control group a continuous, all-you-can-eat fatty-food fiesta for life.
The two groups ate the same amount of food, so the enzyme does not impact appetite. But by 64 weeks, the AdPLA-deficient mice weighed in at a svelte 39 grams, while controls tipped the scales at 74.
For kicks the scientists then repeated the experiment in leptin-deficient mice, with leptin being the hormone that tells your brain you’re full so stop eating. Leptin-deficient mice eat like pigs and put on weight faster than a sumo wrestler on the Oprah Winfrey diet.
Seventeen weeks after this study began, the leptin-deficient mice weighed 75 grams, whereas mice lacking both leptin and functional AdPLA weighed 35 soaking wet.
“This means that local signals in fat tissue allow fat cells to regulate fuel provision for the body, which changes our fundamental understanding of how the body regulates fat breakdown,” Maryam Ahmadian, a study co-author told BurrillReports.
Studies of murine fat metabolism don’t always translate to the human condition, but rest assured that before long someone will take a peek at AdPLA gene expression in humans.
Oh and the AdPLA-deficient mice had significant insulin resistance and a marked increase in liver fat. Somebody needs to get on that, too.