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Pennington Biomedical Discovery Could Pave Way for Better Diabetes TreatmentsNew research debunks previous theories on the role of fat
Released: Tuesday, June 30, 2015
Baton Rouge, LA – Scientists at LSU's Pennington Biomedical Research Center have made a discovery about the way fat is stored and used in the body that could lay the foundation for future development of new treatments for obesity related conditions such as pre-diabetes and diabetes, and for individuals who have an increased risk of heart disease and stroke.
New research from Professor Randy Mynatt and his team shows that mice lacking a certain gene in their skeletal muscle that allows their bodies to burn fat, adapted to burn blood sugar instead. This finding that goes against previously-held theories on the cause of diabetes and insulin resistance.
Researchers previously believed that diabetes and insulin resistance were caused by an accumulation of lipids - or fat - in skeletal muscle, sometimes due to a lack of exercise and the body's inability to burn (or oxidize) that fat. In theory, too much fat in skeletal tissue prevented blood sugar from getting into cells and being burned, which led to insulin resistance and eventually diabetes.
This new discovery disproves that theory by revealing that mice without a gene called CPT1B (which allows fat burning in skeletal muscle) were actually healthier than mice with the gene. Instead of becoming obese, insulin resistant and eventually developing diabetes as Mynatt and his team predicted, mice without the CPT1B gene burned blood sugar and were significantly healthier and leaner than mice that burned fat. Additionally, mice without the CPT1B gene burned more metabolic energy than their counterparts, even with a high-fat diet and less exercise.
"This is kind of like maintaining the same fat mass when we're older that we had as teenagers and having a higher and more efficient metabolism, even with the lifestyle of a couch potato," Mynatt said.
Future research will focus on inhibiting fat usage in skeletal muscle without impacting the heart by targeting specific tissues, which is a challenging prospect according to Mynatt.
"Building on this new discovery, we now want to figure out how our muscles are communicating with the rest of the body so we can develop better therapies," Mynatt said. "The key goal here is to find better treatments for diabetes and perhaps even lead us to a cure."
Mynatt's work entitled, "Impaired mitochondrial fat oxidation induces adaptive remodeling of muscle metabolism" was recently featured in the prestigious Proceedings of the National Academy of Sciences of the United States of America.
You can read the paper here: http://www.pnas.org/content/early/2015/06/03/1418560112.abstract
The Pennington Biomedical Research Center is at the forefront of medical discovery as it relates to understanding the triggers of obesity, diabetes, cardiovascular disease, cancer and dementia. It is a campus of Louisiana State University and conducts basic, clinical and population research. The research enterprise at Pennington Biomedical includes approximately 80 faculty and more than 25 post-doctoral fellows who comprise a network of 44 laboratories supported by lab technicians, nurses, dietitians, and support personnel, and 13 highly specialized core service facilities. Pennington Biomedical’s more than 500 employees perform research activities in state-of-the-art facilities on the 222-acre campus located in Baton Rouge, Louisiana.