A new study conducted by Western University’s researchers revealed that one gene, when removed from mice, might lead to increased fat accumulation. Accordingly, our genetic information might be the cause of obesity.
Scientists at Western University’s Schulich School of Medicine and Dentistry identified a gene that regulates fat accumulation and metabolism in mice subjects. The recent research might shed some light on why some people struggle losing weight while others are fit, regardless of what they’re eating. According to the study, besides an unhealthy diet and lifestyle, genetic information might be the cause of obesity.
“When we removed this gene we see that mice make a lot more fat,” Silvia Penuela, Ph.D., an assistant professor at Schulich. explained in an interview with CBC News.
According to the researchers, we can accumulate fat tissues by either creating more fat cells or by increasing the fat cells already installed in our body.
Genetic Information Might Be The Cause Of Obesity
“So far we can see the fat cells in mice get bigger so that they’re able to accumulate a lot more fat. That is what we saw in the mouse no matter the diet. So if the mouse had a high-fat diet or a regular diet, unfortunately, in both cases they would accumulate the same amount of fat,” Silvia Penuela added.
The gene in question is Pannexin 1, and its absence can also increase the risks of type 2 diabetes.
Of course, we have to see how this plays out in humans so that we can obtain the fat cells from human patients and check the expression of this gene or Pannexin 1. We’re trying to see if we can correlate the amount of Pannexin 1 with the propensity of that patient to accumulate fat and maybe we can draw some conclusions based on that,” Silvia Penuela said.
“We are many, many years from that, unfortunately. But, right now at least we think we can use this as a bio-marker just to see if maybe we can predict certain patients that will have this deficiency or this mutation, that makes them more likely to accumulate fat,” Penuela concluded.