Cardiovascular disease affects millions of Americans every year, and its strongly linked to obesity. A new study from the University of Helsinki has made novel connections between a gene and weight loss in extensive mouse studies. A huge impact could be made on decreasing the prevalence of cardiovascular disease should this study’s findings be translated into a therapy for reducing body fat in obese people.
The team from Helsinki started with a gene called USF1 (Upstream Transcription Factor 1) because of its previous association with lower cholesterol and triglyceride levels in humans. To learn more about the role of USF1 in metabolic health, they removed the gene from mice and examined their blood lipid profile. This is what they found:
- Low levels of triglycerides
- High levels of HDL cholesterol (the “good” kind)
The above ratio of triglycerides to HDL cholesterol is unhealthily opposite in obese people, so the researchers were quickly excited about the potential of their findings of USF1 impact. Even more, the USF1 knock-out mice remained lean even after being fed a fatty diet. In comparison to control mice with perfectly normal USF1 expression, the two group ate and exercised the same amount, but the USF1 knock-out mice weighed half as much as the control mice.
With the next step in their research being identifying the characteristic of USF1 that results in weight loss in its absence, the team noticed that the USF1 knock-out mice were consuming increasing amounts of oxygen and subsequently producing more carbon dioxide, indicating their metabolic rate had increased after losing USF1 expression. Then, they were able to connect the heightened metabolism to “brown fat.”
Brown fat actually burns fat for the purpose of generating heat to protect mice from cold temperatures. Humans also have brown fat. When USF1 was missing, the brown fat in the knock-out mice burned fat and sugar even at room temperature, like an “efficient vacuum cleaner.”
In humans, the same researchers found a less active form of USF1 that has similar, if less drastic, effects on humans as on mice with the gene knocked out.
Further studies on USF1 inhibition in humans could greatly help people dealing with multiple health problems relating to obesity and type 2 diabetes.
Source:
University of Helsinki
