Fat Cells Produce Appetite-Stimulating Hormone That Drives Weight Regain, Scientists Discover

The Signal Behind Increased Appetite

According to НВ — Техно: Researchers at the Harrington Discovery Institute, affiliated with University Hospitals and Case Western Reserve University, have uncovered a biological mechanism explaining why lost weight often returns. This process involves the hormone asprosin, secreted by fat cells, which signals the brain to boost hunger. Their study revealed that epigenetic modifications, particularly involving the molecule TGF-β1, sustain elevated production of asprosin even after weight loss.

Using mice as a model, scientists found that fat cells continue to produce high levels of asprosin following weight reduction. The team identified a molecular “memory” in fat cells caused by prior obesity, which leads to persistent increases in this hormone. Remarkably, even mice that had fully shed excess weight still showed heightened asprosin secretion.

Epigenetic Changes and Their Impact

The molecule TGF-β1 triggers epigenetic alterations-changes that do not modify DNA sequences but influence gene activity. These modifications remain stable even after TGF-β1 levels return to normal. Blocking asprosin production or its brain receptors in mice prevented weight regain after dieting. The findings also suggest this mechanism could pass an increased risk of obesity to offspring.

Preliminary human studies have partially validated these results, though further research is needed to deepen understanding. Current appetite-suppressing treatments like GLP-1 receptor agonists reduce hunger during use but do not reverse the epigenetic changes in fat tissue. Future trials aim to evaluate therapies that block asprosin or its epigenetic effects, potentially in combination with GLP-1 drugs or following their discontinuation.

Independent laboratories have confirmed some of these findings. Cross-analysis of human and mouse data provided additional support for the identified mechanism. While most experiments have been conducted in mice, ongoing human studies seek to confirm and expand on these insights.

Identifying asprosin’s role and the accompanying epigenetic changes in obesity-related processes holds promise for developing treatments to prevent weight regain.

Understanding how fat cells retain this "molecular memory" opens new avenues for therapies targeting long-term weight management. Continued human research will be crucial to verify these discoveries and translate them into effective clinical interventions. This breakthrough marks a significant advance toward improved strategies for combating obesity and its related health issues.

Understanding the mechanisms behind weight regain is crucial, especially when considering recent findings that just one week of strength training can stimulate the breakdown of harmful visceral fat. This highlights the importance of integrating exercise into weight management strategies. For more insights on how physical activity can impact fat loss, check out our article on the effects of strength training on visceral fat.