Turning off the function of a single protein-coding gene — called USF1 — could offer insight into how to treat a handful of cardiometabolic diseases like obesity, diabetes, and atherosclerosis. Lessening the gene’s expression activates calorie-burning brown fat, keeping mice lean even when they’re fed a high-fat diet. Here’s what lead researcher Dr. Pirkka-Pekka Laurila of the University of Helsinki said about the findings, published in the new Science Translational Medicine.
What happens when you block USF1’s expression?
When USF1 expression is blocked in mice, the mice are protected against weight gain, even when fed a high-fat diet. In humans, individuals who had a lesser amount of USF1 gene product improved their lipid levels, were more insulin sensitive, and developed fewer plaques in the arteries.
How did that impact fat in the body?
When USF1 was inactivated in the mice, the brown adipose [fat] tissue became more active in burning fats and lipids. It cleared sugar and triglycerides more rapidly from the circulation, improving blood lipid levels.
What’s the potential usefulness of that finding?
These findings suggest that USF1 could be a therapeutic target for cardiovascular and metabolic disease. Genes have evolved to serve well-defined functions in our bodies. How can loss of USF1 be beneficial for metabolism? In the Paleolithic period, with a cycle of famine and feast, USF1 might have been an important player in storing energy. In the current world, with constant feast, the energy-storing function of USF1 might be redundant.
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