No one may ever need to get fat again, thanks to research conducted by scientists at Virginia Tech University.
The keys to the discovery are tiny strands of RNA that regulate how our body burns fat and sugar. The researchers found that mice on high-fat diets were resistant to becoming obese when two mini-molecules called microRNAs were missing from their genetic makeup, reports HealthCanal.com.
The breakthrough — summarized in a paper published in the Proceedings of the National Academy of Sciences — suggests that the nation’s obesity epidemic could be addressed if treatment targeted the two specific microRNAs. About one-third of adults in the United States and 17% of the nation’s children are obese, raising their risk of contracting type 2 diabetes, heart disease, a stroke, liver disease, and some cancers, according to the National Institutes of Health.
“Scientists know the best health solution for obesity involves eating less and exercising more,” says Matthew W. Hulver, associate professor with the Department of Human Nutrition, Foods, and Exercise in the College of Agriculture and Life Sciences at Virginia Tech. “But in cases when people can’t or won’t exercise, if we can identify what is contributing to the regulation of our metabolic circuits, we can target it with a drug or pharmacologic solution.”
Virginia Tech — with departments managing a research portfolio of $450 million and concentrating on energy, materials, environmental, innovative technology, and health research — is often ranked as one of the best graduate schools in the nation. In fact, it hosted the World Polymer Congress, attended by award-winning scientists from about 70 countries, last June. Its home is in Blacksburg, VA, which is recognized as one of the best towns to raise children and start small businesses.
MicroRNAs were once considered by scientists to be little more than scrap DNA, but now they are believed to have an important role in regulating how genes shape human health and behavior. While researchers have thought microRNAs were linked to problems with obesity, the new findings established for the first time a connection between the strands and cellular metabolism.
Virginia Tech partners in the research, the biologists at University of Texas (UT) Southwestern Medical Center in Dallas, modified mice to be genetically unable to produce microRNA-378 and its cousin, miR-378. The result was that mice stayed slender and had metabolisms that quickly converted cellular food into energy.
Eric N. Olson, Ph.D., professor and the chairman of molecular biology at UT Southwestern and senior author of the study, says:
We did not know the function of this pair of microRNAs, but were intrigued because they arose from a gene connected with metabolism, and they are expressed in a variety of tissues, such as muscle, fat, and liver. When we modified mice so that they were missing these microRNAs, it permitted their cells to burn more energy and have greater obesity resistance than those of their untreated litter mates. This pair of microRNAs seems to function as key regulators of metabolism, suggesting that a drug designed to inhibit them would have a positive effect against obesity.
In their research, Virginia Tech scientists isolated mitochondria — the engines in cells that turn fat and other fuel into energy — from liver and skeletal muscle. When they measured the mitochondria’s use of fatty acids, they found that a chemical process that releases energy energy, called oxidation, was increased. This discovery supported the notion that the loss of microRNAs results in increased energy expenditure and resistance to obesity, even with a high-fat diet, the researchers believe.
Dr. Gerald W. Dorn II, the Philip and Sima K. Needleman professor of Medicine at Washington University School of Medicine in St. Louis, who did not participate in the research, says:
The take home message is microRNAs potentially are a magic bullet against obesity. This is a surprising finding that sheds light on how the body processes food and, in this case, how mice are able to withstand a fat-laden diet and stay skinny. In perspective, people evolved to be able to survive starvation, but as a culture, we’re never much farther than a quarter a mile away from McDonald’s. It would be nice to tinker with the metabolic gene program, and this research provides a single target that affects how the body deals with energy.
Dale McGeehon has been a journalist and editor for more than 25 years, covering chemical regulation and testing for Pesticides and Toxic Chemical News and innovations in material sciences for the National Technology Transfer Center. His writing credits include Omni and College Park magazines and The New York Times.