The researchers say that making a protein called USF1 disable may open up a new way of treating cardiovascular metabolic diseases ranging from diabetes to obesity and atherosclerosis and fatty liver disease.
New study shows that blocking USF1 can protect mice suffering from these diseases, but people also tend to reduce the expression of USF1 are protected. USF1 is a transcription factor gene expression, it is a genetic disease and coronary heart disease and high cholesterol and fat are associated. However, whether the protein will lead to or protect the body against these diseases have been confusing you. When mice lack Usf1 research, Pirkka-Pekka Laurila and colleagues found, USF1 loss can produce a wide range of metabolic benefit. They even fed high-fat diet, mice lacking Usf1 also leaner than normal mice and lower blood lipid levels. Mice lacking Usf1 also more sensitive to insulin, the liver less fat, less artery-clogging plaque occur. The researchers attributed these benefits they have more active brown adipose tissue, which is often called "good" fat. And white adipose tissue (which will store excess fat) is different, and brown adipose tissue to generate body heat will burn fat. Order Usf1 disability seems to activate brown adipose tissue, stimulate it and burn more fat intake, which in turn can remove blood lipids.
The researchers also found that, compared with normal people, people who has reduced expression of the gene USF1 carrying mutant has better lipid metabolism. What's more, their blood has more "good" cholesterol and less fat. And it is also unlikely for them to have insulin resistance and arterial blockage.
In conclusion, these findings with USF1 gene may lay the foundation of treating heart disease, obesity and other metabolic diseases.
Related reading: http://www.cusabio.com/Polyclonal-Antibody/ATL3-Antibody-11098193.html
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