Obesity is a increasing problem in many countries. Obesity is a chronic, medical condition that a person has an abnormal accumulation of body fat, usually 20% or more over the ideal body weight. Obesity is defined as a BMI of 30 or higher. A certain amount of body fat is necessary for various functions like energy store, but too much body fat can cause a broad range of health problems, such as type 2 diabetes, high blood pressure, and high cholesterol.
Excessive fat weighs down not just your body, but also your brain. The brain is known to be involved in development. However, the exact mechanism of how an unhealthy diet alters the brain and thus leads to body fat accumulation remains unclear. Now, a study published September 13 in the journal Cell Reports has revealed a novel mechanism in the mouse brain that modulates obesity, providing a potential therapeutic target for the intervention of obesity.
Researchers looked at the Rap1 gene in mice. This gene is important for brain functions such as learning and memory, but how it influences energy balance is not clear. To determine the effect of brain Rap1, researchers used two groups of mice: the experimental group in which the mice lacked the Rap1 gene, and the control group in which the mice carried a normal Rap 1 gene. Both groups were fed on a high-fat diet. To their surprise, researchers observed a significant reduction in body weight and body fat in mice without Rap 1. By contrast, the control group gained weight. When given a normal diet, mice in both groups had similar weights and body fat.
Study senior author Dr. Makoto Fukuda said that the mice without the Rap1 gene ate less and burned more fat compared to mice with that gene, and the mechanism involving brain Rap1 might be a target for the intervention of obesity.
About Rap1
The Rap1 gene encodes a protein that belongs to the Ras family of small GTPases.
RAP1 is a gene that also protects telomeres. This study shows that Rap1 plays a central role in dietary obesity, glucose imbalance, peripheral insulin resistance, and central leptin resistance. CusAb offers Recombinant AGTR1 and Rap1.
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