Obesity has become a global epidemic, with the number of people affected nearly tripling since 1975. While lifestyle factors like diet and exercise contribute to obesity, scientists have discovered that intrinsic metabolic abnormalities are also associated with this condition.
In a breakthrough study, researchers from the University of California San Diego School of Medicine have shed light on how obesity affects the mitochondria, the vital energy-producing structures within our cells.
The study, published in Nature Metabolism, involved feeding mice a high-fat diet and observing the impact on their fat cells’ mitochondria. The researchers found that the mitochondria in the fat cells broke apart into smaller, less efficient mitochondria that had reduced fat-burning capacity. Remarkably, this process was controlled by a single gene.
By deleting this gene from the mice, the researchers were able to protect them from excess weight gain, even when they consumed the same high-fat diet as the other mice. This research highlights the critical role of this gene in the transition from a healthy weight to obesity.
Alan Saltiel, a professor in the Department of Medicine at UC San Diego School of Medicine, explains that caloric overload from overeating leads to weight gain and triggers a cascade of metabolic changes that further reduce energy burning, exacerbating obesity. The identified gene plays a crucial part in this transition.
Obesity occurs when the body accumulates excessive fat, primarily stored in adipose tissue. While adipose tissue provides mechanical benefits such as cushioning vital organs and insulation, it also has important metabolic functions. These include releasing hormones and signaling molecules that regulate energy storage and burning in other tissues.
In the case of obesity, fat cells lose their ability to effectively burn energy, making it challenging for individuals with obesity to lose weight. Understanding how these metabolic abnormalities develop is a significant area of study in obesity research.
The researchers fed mice a high-fat diet and monitored the impact on their fat cells’ mitochondria, which help burn fat. They made a unique observation: after consuming the high-fat diet, the mitochondria in certain parts of the adipose tissue fragmented, forming smaller and less efficient mitochondria that burned less fat.
Additionally, the researchers identified a molecule called RaIA that played a crucial role in this metabolic effect. RaIA is involved in breaking down dysfunctional mitochondria. When this molecule is overactive, it interferes with the normal functioning of mitochondria, triggering the metabolic dysfunctions associated with obesity.
The study suggests that chronic activation of RaIA suppresses energy expenditure in obese adipose tissue. By understanding this mechanism, researchers are one step closer to developing targeted therapies that increase fat burning and address weight gain and associated metabolic dysfunctions.
This groundbreaking research provides valuable insights into the mechanisms behind obesity-related metabolic dysfunction. It offers hope for the development of targeted treatments that can effectively address the global obesity epidemic.
1.Source: Coherent Market Insights, Public sources, Desk research
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