How a Gene could be Responsible for Obesity
Could it really be as simple as blaming a gene for the obesity crisis everywhere? If so, then maybe it's not even your fault that you're overweight. And then maybe in a few years we all can be normal weight after undergoing a gene therapy.
The Medical Daily published the results of a study that specifically explored the role of the Rap1 Gene when it comes to obesity. Read the story below.
A new mechanism that could potentially be used as a target to treat obesity has been discovered in mice models by scientists, latest research shows.
For the study, published in the journal Cell Reports on Tuesday, scientists from Baylor College of Medicine, the National Institutes of Health and Virginia Tech Carilion Research Institute looked at the Rap1 gene in mice — expressed in the brain besides other tissues — to gauge its role in energy balance.
“It’s well known that the brain is involved in the development of obesity, but how a high-fat diet changes the brain so it triggers the accumulation of body fat is still unclear,” said senior author Dr. Makoto Fukuda, assistant professor of pediatrics at the Texas-based Baylor College of Medicine, in a press release.
The researchers studied two groups of mice — one group was genetically engineered by selectively deleting the Rap1 gene in a group of neurons in the hypothalamus, while the other was used as a control group. Both groups were then fed a high-fat diet (60 percent of the calories coming from fat).
While the control mice gained weight, the mice without the Rap1 gene had reduced body weight. When both groups were fed a normal diet, they showed similar weight and body fat.
“We observed that the mice lacking Rap1 were not more physically active. However, they ate less and burned more body fat than mice with Rap1,” said Fukuda. “These observations were associated with the hypothalamus producing more of a hormone that reduces appetite, called POMC, and less of hormones that stimulate appetite, called NPY and AgRP.”
The genetically engineered mice also registered lower levels of blood glucose and insulin than the control group.
The scientists also studied the mice’s response to leptin — the "satiety hormone" — and found that the high-fat diet did not lead to the engineered group developing leptin resistance. Leptin resistance is one of the most common signs of obesity in humans.
In other tests, they tried to inhibit Rap1 with drugs, as opposed to deleting the gene in the mice with inhibitor ESI-05. Fukuda observed, “When we administered ESI-05 to obese mice, we restored their sensitivity to leptin to a level similar to that in mice eating a normal diet. The mice ate less and lost weight.”
“This new mechanism involving Rap1 in the brain may represent a potential therapeutic target for treating human obesity in the future,” said Fukuda.