Researchers at UT Southwestern Medical Center have taken another step toward better understanding the metabolic functions of obesity and its connection to type 2 diabetes.
Dr. Philipp Scherer, Director of the Touchstone Center for Diabetes Research at UT Southwestern, led a group of researchers in a recent multicenter study published in Nature Medicine that successfully identified ways to manipulate the protein mitoNEET. This is the first time the protein has been effectively altered to expand fat tissue in a way that allows subjects - in this case, mice - to remain metabolically healthy.
MitoNEET is a key component of a cell's mitochondrion, which serves as the cell's energy powerhouse. When the levels of MitoNEET protein were elevated inside the fat cells of rodents, more fat was stored in the adipose tissue, thereby keeping toxic lipids away from other types of cells. This sequestration resulted in extremely obese yet metabolically healthy mice that displayed no signs of type 2 diabetes. In contrast, when MitoNEET levels were decreased, the mice became lean but unhealthy, and developed pre-diabetic conditions such as failure to metabolize glucose properly.
"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 our weight," said Dr. Scherer, senior author of the three-year study and Professor of Internal Medicine and Cell Biology at UTSW.
The body stores fat in the white adipose tissue, and, ideally, individuals burn any excess calories through exercise and a healthy diet. The current research findings suggest that manipulating components of mitochondria in fat cells can be an effective way to funnel excess calories into "good" locations. This storage then thwarts their negative effect on other internal organs like the liver in which excess fat accumulation is toxic.