Obesity gene discovery: scientists edge closer to breakthrough in weight gain fight

The latest research by scientists from the University of California San Diego, published in the journal "Science", indicated that mice fed a high-fat diet experienced issues with their mitochondria. These structures deteriorated into smaller fragments, hindering the efficient burning of fat.

Mitochondria are cell structures that facilitate fat burning. They play a crucial role in metabolism, transforming food into energy through adenosine triphosphate (ATP) molecules. The higher the number of efficient mitochondria in the body, the more influential the process of converting fat into ATP.

The research found that in mice, a high-fat diet reduced the number of properly functioning mitochondria. Additionally, scientists attributed this occurrence to a specific gene. Mice did not experience excessive weight gain when this gene was removed despite consuming the same fat-rich diet as other mice.

Fat tissue serves several vital functions in the body, such as maintaining body temperature, providing insulation and cushioning for internal organs, and influencing and producing hormone release. The ideal fat percentage in women's bodies is 23-34%, and in men's bodies, it's 8-20%. However, significant overconsumption of calories leads to excess energy being stored as triglycerides in adipocytes, the cells that constitute fat tissue. This causes fat cells to enlarge, fat tissue to expand, and body weight to increase, ultimately resulting in overweight and obesity.

"The excessive caloric intake from overeating can lead to weight gain and trigger metabolic processes that reduce energy expenditure, further escalating obesity," explains Dr. Alan Saltiel, an endocrinologist and biochemist from the UC San Diego School of Medicine.

The researchers discovered that obesity diminishes fat cells' ability to burn energy, making weight loss more challenging for obese individuals. To understand why this occurs, scientists fed mice a high-fat diet and studied its impact on their fat cells' mitochondria. They found that under such a diet, some mitochondria split into smaller ones, which burned significantly less fat.

The scientists also revealed that the activity of a single molecule, RaIA, drives this mechanism. This molecule has numerous functions, including aiding in the breakdown of mitochondria when they malfunction. It appears that when RaIA is overactive, it disrupts normal mitochondrial functioning and triggers their fragmentation, leading to metabolic disorders associated with obesity.

"The excessive activity of RaIA plays a pivotal role in reducing energy expenditure in the fat tissue of obese mice. Understanding this mechanism brings us closer to developing therapies that could counteract weight gain and related metabolic disorders," explains Dr. Saltiel.

When researchers removed the RaIA-related gene from the mice, their body weight did not increase, despite being on a high-fat diet. The scientists also suggested that some proteins affected by RaIA in mice closely resemble human proteins linked with obesity and insulin resistance. This similarity implies that analogous mechanisms may cause obesity in humans and animals.

"Comparing the results of our research with clinical data from individuals could help us in treating or preventing obesity. We are just beginning to understand this complex disease's metabolism, but the potential future breakthroughs are promising," says Dr. Alan Saltiel.

Obesity, considered a chronic disease by the World Health Organization, affects more than 20% of the global population, and over 4.5 million people die prematurely as a result. Experts foresee that by 2030, one billion people will be afflicted with this disease. About 60 Poles, including one in ten children, are currently battling overweight and obesity.