Researchers at Sanford-Burnham Medical Research Institute say they’ve found a key factor behind the inflation of our waistlines. It’s a little protein called p62 (not to be confused with P90X), and without it, our bodies start storing fat without burning energy p62 Links β-adrenergic input to mitochondrial function and thermogenesis. Müller, T.D., Lee, S.J., Jastroch, M., et al. The Journal of Clinical Investigation 2013;123(1):469-78. . As much as we’d like to rejoice, there's one caveat: the research was on mice, not people, so it’s unclear if the findings can apply to humans.
Why It Matters
The experiments were complicated. Scientists created mice missing p62 in specific types of tissue, such as central nervous system and liver, and found that these mice weren’t obese. Next, researchers produced mice that were missing p62 only in their adipose (fat) tissue. Sure enough, the mice blew up like balloons at a Thanksgiving Day parade. And it wasn’t a result of scarfing down chunks of cheese. Study co-author Dr. Jorge Moscat says the effects of p62 activity don’t have anything to do with diet or exercise Mature-onset obesity and insulin resistance in mice deficient in the signaling adapter p62. Rodriguez, A., Durán, A., Selloum, M., et al. Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Madrid, Spain. Cell Metabolism 2006;3(3):211-22. .
The conclusion? When p62 is absent from fat tissue, the body’s metabolic balance changes. So the body stops producing brown fat, a type of fat that burns energy, and generates more white fat, which stores energy. The study authors say these findings could pave the way for new treatments for obesity (in humans, that is).
Is It Legit?
Maybe. After all, it’s only been tested in mice so far. In earlier studies, the scientists engineered mice missing the p62 protein in all types of tissue and found that the mice quickly became obese. Other research (also on rodents) points to p62 as a culprit behind insulin resistance as well as obesity A functional role for the p62–ERK1 axis in the control of energy homeostasis and adipogenesis. Lee, S.J., Pfluger, P.T., Kim, J.Y., et al. Department of Cancer and Cell Biology, The Vontz Center for Molecular Studies, University of Cincinnati College of Medicine, Cincinnati, Ohio. EMBO Reports 2010;11(3):226-32. Sequestosome 1/p62, a scaffolding protein, is a newly identified partner of IRS-1 protein. Geetha, T., Zheng, C., Vishwaprakash, N., et al. Department of Nutrition, Dietetics, and Hospitality Management, Auburn University, Auburn, AL. The Journal of Biological Chemistry 2012;287(35):29672-8. .
The researchers believe the human body could react similarly, and they’re currently running trials on patients with metabolic disorders. Ultimately, Moscat says he and his co-authors believe p62, among other proteins, can be a “therapeutic target for obesity and type 2 diabetes.”
Still, it’s important to note no one’s saying the absence of p62 is the sole cause behind obesity. There are lots of genetic and lifestyle factors, including diet and exercise, that play a role in weight gain. But the more information we have, the better we can fight the spread of a growing health issue.
Do you think there's a genetic component to obesity? Let us know in the comments below or tweet the author directly at @ShanaDLebowitz.