A recent study, published in the Proceedings of the National Academy of Science, has revealed that there is a link between cellular metabolism and microRNAs. This indicates that a medication developed to hinder these small molecules may work to fight obesity.
RNA influences how our cells burn sugar and fat, a discovery which has given the experts from Virginia Tech and the University of Texas Southwestern Medical Center at Dallas a jump start for finding methods of treating obesity and other weight-related health concerns.
The researchers have found that when 2 microRNAS (“mini-molecules”) are absent from mice’s genetics, they become immune to obesity, which suggests that treatment aimed at microRNAs could help the obesity pandemic hitting the world.
The WHO (World Health Organization) said that in 2008, around 500 million adults were obese, and in 2010, more than 40 million children under the age of 5 were overweight as well.
The National Institutes of Health stated that between 2009 and 2010, over 12.5 children and 78 million adults were obese, which severely increased the risk of heart disease, stroke, liver disease, cancer and type 2 diabetes.
Matthew W. Hulver, Ph.D., an associate professor with the Department of Human Nutrition, Foods, and Exercise at the College of Agriculture and Life Sciences at Virginia Tech, commented:
“Scientists know the best health solution for obesity involves eating less and exercising more. But in cases when people can’t or won’t exercise, if we identify what is contributing to the regulation of our metabolic circuits, we can target it with a drug or pharmacologic solution.”
Scientists previously believed that microRNAs were merely “scrap DNA”, however, they now understand its importance for controlling how genes determine human behavior and health.
MicroRNAs have been associated with:
- breast cancer
- heart disease
Prior trials have connected microRNAs and obesity, however, the new research has found an association between them and cellular metabolism.
Scientists at UT Southwestern Medical Center altered the genetics of mice so that they were not able to make microRNA-378 or its cousin, miR378*, which results in slim animals with fast metabolisms that transform cellular food to energy.
Eric N. Olson, Ph.D., senior author of the trial, a professor and the chairman of molecular biology at UT Southwestern, added:
“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 to 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.”
The team analyzed the outcomes of the microRNA alterations on different disease conditions, such as amyotrophic lateral sclerosis (Lou Gehrig’s) and heart disease.
During the present study, researchers from Virginia Tech, Madlyn I. Frisard, Ph.D, an assistant professor of Human Nutrition, Foods, and Exercise, and Hulver, Metabolic Phenotyping Core director at Virginia Tech, took mitochondria, which is responsible for turning fat into energy, away from the liver and skeletal muscle.
After measuring mitochondrial use of fatty acids, a chemical process was discovered. Oxidation became increased, which meant that the researchers were correct in believing that the loss of microRNAs makes for an energy increase, and a reduced chance of obesity.
Gerald W. Dorn II, M.D., the Philip and Sima K. Needleman professor of Medicine at Washington University School of Medicine in St. Louis, concluded:
“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,” said Gerald W. Dorn II, M.D., 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. “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.”
Written by Christine Kearney