Scientists from the University of Colorado identified histone deacetylase 11 (HDAC11), an epigenetic modifier, as a way to improve fat burning in overweight mice.
Among mice that were fed a high-calorie diet, deleting HDAC11 improved insulin sensitivity, reduced obesity and stimulated the formation of brown fat tissue, which helps to burn fat.
Significantly, the absence of HDAC11 also triggered beiging of white fat tissue, which stores fat, helping to improve the fat-burning process.
While this discovery is intriguing, its implications for treating obesity and type 2 diabetes are as yet unknown. It could take years for researchers to verify these findings in human trials and achieve similar success, and then a drug that inhibits HDAC11 would have to be developed and tested.
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For the researchers, the next step is to test HDAC11 deletion in larger trials. They also want to explore an associated protein called bromodomain-containing protein 2 (BRD2) in the control of fat burning.
"Through our investigation we found that inhibiting HDAC11 increases energy expenditure, which highlights its potential as a target in obesity and metabolic disease therapeutic strategies," said first author Timothy A. McKinsey, PhD.
"We now need to test the role of HDAC11 in large animal models of metabolic disease and in human cell systems as we attempt to translate these exciting findings to the clinic."
The results have been published online in JCI Insight, a journal published by the American Society for Clinical Investigation.
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