Almost everyone has a friend with a hollow leg. You know, that guy or girl who eats tons, never exercises, and somehow (infuriatingly) stays thinner than a clean eater, a vegan, or a paleo fiend? A new study on mice says it’s all about the (skinny) genes.
What’s the Deal?
Scientists from the University of Sydney were playing around with Kruppel-Like Factor 3 (aka KLF3), a protein that turns various genes off and on, when they made an interesting discovery Mammalian Kruppel-like factors in health and diseases. McConnel BB, Yang VW. Departments of Medicine and of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, Georgia, USA. Physiological Reviews. 2010 Octoer; 90(4):1337-81. . As part of the experiment, the researchers bred mutant mice that could not produce KLF3. They were surprised to find that regardless of food intake, these lab animals didn’t pack on the pounds (or, in this case, ounces).
Why were the mice able to stay so skinny, even when put on a high-fat diet? After looking more closely at KLF3 and its effects, researchers noticed the mutant mice had much higher levels of adipolin, a hormone produced by fat cells which regulates blood glucose. In general, higher adipolin levels mean less fat, because the body is able to better regulate its blood glucose level and prevent all that extra glucose from turning to blubber Adipolin/C1qdc2/CTRP12 protein functions as an adipokine that improves glucose metabolism. Enomo T, Ohashi K, Shibata R, et al. Department of Cardiology, Nagoya University Graduate School of Medicine, Nayoga, Japan. The Journal of Biological Chemistry. 2011 October 7;286(40):34552-8. . KLF3’s main role is to turn genes off and on — in the mutant mice, production of adipolin skyrocketed when there was nothing telling the body to stop producing it. Basically, the extra adipolin acted as a glucose moderator, enabling the mutant KLF-less mice to chow down on more food without getting more fat.
Is it Legit?
Maybe. While this study is fascinating, it’s hard to make any grand sweeping statements without first duplicating the experiment on Homo sapiens. We know that mice can make lousy human substitutes for drug testing, but previous experiments on obesity and genetics have indicated that the gap between mice and men might not be so huge. The research is still in the very earliest stages — scientists need to fully understand how KLF3 and adipolin affect humans before we start touting adipolin as the new anti-obesity wonder drug. But there’s a light at the end of the tunnel. If increased adipolin levels can prevent mice from becoming overweight, it’s very possible that it can do the same in humans.
Do you think conducting studies on mice is an effective way to develop new treatment options for diabetes and obesity? Why or why not? Share your thoughts in the comments below or tweet the author @SophBreene.