NOT THAT FAT: Scientists have found a fat-based hormone that causes the body's fat cells to make "homemade fat"--which they say improves protects against metabolic diseases. Image: © ISTOCKPHOTO/MATT JEACOCK
Scientists have stumbled on a chemical in the body that could one day prevent or reverse diseases linked to obesity.
Researchers at Harvard University's School of Public Health (H.S.P.H.) report in Cell that palmitoleate, a newly discovered hormone produced by fat cells, is also a fatty acid. (Most hormones are proteins.) They believe that if they can increase its production, they may be able to stave off metabolic diseases such as diabetes, heart disease (caused by hardening of the arteries) and so-called fatty liver, an often asymptomatic disease that can lead to damage of the organ as well as cancer. They speculate that it may also aid in weight loss.
But how could fats help trim the portly—or at least avoid accompanying diseases?
"The homemade meal is always the healthiest and best tasting meal," says study co-author Gökhan Hotamisligil, a professor of genetics and metabolism at H.S.P.H. "Similarly, the best kind of fat is the kind that you produce on your own from your fat tissue."
He says researchers discovered palmitoleate's potential thinning power by engineering mice that did not have proteins responsible for shuttling dietary fat to storage fat cells (often found around the abdomen, thighs and other places familiar to cellulite hosts). The animals ate like pigs, so to speak, but remained lean, free of metabolic disease, and showed no sign of fat deposits on their livers or insulin resistance. (Resistance to insulin—a hormone produced in the pancreas—causes sugar to accumulate in the blood instead of being taken up the muscle, which can result in type 2 diabetes.)
Hotamisligil says the team traced the hormone to fat cells when they were trying to figure out why these mice had so many fat molecules in their blood. Normally, excess of fatty acids in the bloodstream end up in the muscle and liver—and eventually affect insulin-sensing cells, causing diabetes.
"Fat is a huge soup of many many chemical entities," Hotamisligil says. "You can't treat fat like one kind of thing. It's a combination of many different kinds of molecules—the composition of [the] soup is important."
Palmitoleate is involved in a process known as de novo lipogenesis, the production of fat molecules by fat cells. The naturally made fat, he explains, appears to have the opposite effect of fat from food: It actually keeps fat from accumulating on the liver and thwarts insulin resistance. He noted that whereas the healthy rats had lots of palmitoleate in their fat reserves, diabetic mice do not. The mechanism by which palmitoleate works, however, has yet to be figured out.
"If you can replenish that source [of palmitoleate] or find a way to activate fat cells to produce more of their own fat, this could end up helping people with obesity, diabetes and fatty liver disease," says Hotamisligil.
He warns that high palmitoleate levels may only guard against metabolic illness and not obesity itself. Although he cannot be certain that the hormone has the same effect on humans, he does note that the pathways involved in mice and humans are almost identical.
In an editorial accompanying the Cell article, endocrinologist Jerrold Olefsky of the University of California, San Diego School of Medicine points out: "Earlier studies have indicated that the capacity of human [fat cells] for de novo biosynthesis of fatty acids is considerably less than in rodent models." More work has to be done, he says, to determine if higher palmitoleate levels coincide with less metabolic disease in humans, as well.