If you’ve been stuck on a weight loss plateau for months, you’re not alone. Many people find that after initially shedding pounds, the process becomes significantly harder. This is often due to the body entering “starvation mode,” where metabolism slows down, and fat storage increases rather than burning fat for energy. This phenomenon can even occur with medications like Ozempic and Wegovy, which are known to help in weight loss but often see diminishing returns after a 20% to 25% weight loss—leading to what’s known as the “Ozempic plateau.”
However, a recent breakthrough from researchers at the University of Southern Denmark could offer new hope for those struggling to push past this barrier. A study published in Cell Metabolism suggests that it may be possible to control the metabolic adaptations that lead to weight loss stalls.
Kim Ravnskjaer, a molecular biology professor and lead author of the study, explained that weight loss typically progresses well at the beginning but slows down as the body adapts to the changes. He and his team investigated the role of a specific gene, Plvap, in the liver’s metabolism of fats and sugars.
Previous studies had shown that individuals without this gene experience challenges in lipid metabolism—the breakdown and utilization of fats for energy. Ravnskjaer’s team wanted to understand this further and explore how it might affect weight loss.
Their research on mice revealed that Plvap plays a significant role in the metabolic shift from burning sugar to burning fat, especially during fasting or “starvation mode.” In the lab, when the gene was deactivated, the liver failed to recognize the fasting state, continuing to metabolize sugar instead of switching to fat-burning mode. This discovery raises the possibility that it may be possible to “trick” the body into maintaining a faster metabolism.
“If we could develop a medication that helps maintain the burning of fat and sugar at a high rate throughout weight-loss treatments, it could help people break through the common weight-loss plateau,” Ravnskjaer said.
Excitingly, the research also suggested that by manipulating this gene, weight loss medications and diabetes treatments could become more effective. The mice in the study experienced no negative effects, and in fact, showed lower blood sugar levels and improved insulin sensitivity—key markers for potential benefits in diabetes management.
Ravnskjaer highlighted the relevance of the findings for type 2 diabetes patients, explaining that better regulation of blood sugar could help manage the chronic complications often associated with the condition. While this research is promising, it’s important to note that it has only been conducted in mice so far, and human trials are still a long way off.
“There is still a long journey from these mouse experiments to a marketable drug,” Ravnskjaer acknowledged. “However, the potential for this research is clear.”
For now, the discovery offers a glimmer of hope for those caught in the frustrating cycle of weight loss stalls, as well as for individuals struggling to manage blood sugar levels in diabetes.
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