Research results were released that make a clearer understanding of the metabolic functions of obesity and its connection to Type 2 diabetes. Research studies are ongoing in regards to using this data about the protein mitoNEET in hopes of creating different medications for the treatment of diabetes.
The protein “mitoNEET” is a major part of the cell’s mitochondrion, which is the cell’s energy powerhouse. MitoNEET binds pioglitzaone (Actos TM) an insulin-sensitizing drug that is used in the treatment of Type 2 diabetes.
Dr. Philipp Scherer, Director of the Touchstone Center for Diabetes Research at UT Southwestern, headed a group of researchers in a recent multicenter study, the results of which were published in Nature Medicine, that found ways to manipulate mitoNEET. In this study, it indicated that this is the first time mitoNEET has been altered to expand fat tissue that allowed the study models (mice) to remain metabolically healthy. As the mitoNEET levels were elevated inside the fat cells of the mice, more fat was stored in the adipose tissue; thus, the toxic lipids were kept away from other types of cells. Due to this separation, and the resultant toxic lipids staying away from other cells, the results were a very obese (fat) mouse, but a metabolically healthy mouse (a mouse with no symptoms of Type 2 diabetes). In contrast, when mitoNEET levels were decreased, the mice lost weight but were unhealthy mice that developed pre-diabetic conditions, i.e., the inability to process glucose properly.
Dr. Scherer, senior author of the three-year study and Professor of Internal Medicine and Cell Biology at UTSW, stated: “The manipulation of mitochondrial activity in fat tissue is a very powerful approach to control how much excess energy we store in our bodies and where we store it. We have heretofore underestimated the importance of mitochondrial pathways in our fat cells and their influence on how we manage weight.”
With a healthy diet and exercise, the body hopefully stores fat in the white adipose tissue. Research indicates that by changing the components of mitochondria in fat calls can be an effective way to funnel extra calories to good locations. This would stop the bad effect on other organs of the body, like the liver, where fat would accumulate. Those working on the study stressed that the findings were not supposed to encourage obesity, even though the fat mice were considered to be metabolically healthy.
It is hoped that the results of this study can now be used in a clinical setting in the development of future treatments.
The study was funded by support from the National Institutes of Health, the American Heart Association, and fellowships from the Juvenile Diabetes Research Foundation and the Department of Defense.
