Tokyo, Japan – A groundbreaking study from the University of Tokyo reveals that obesity causes temporary, but not permanent, disruptions in the liver’s ability to adapt to starvation. Published in Science Signaling, the research provides crucial insights into metabolic resilience and opens new avenues for understanding obesity-related diseases.
Key Findings
- Obesity temporarily impairs the liver’s starvation-response network but does not destroy its underlying structure.
- Healthy livers rely on ATP and AMP (key energy regulators) to coordinate metabolic timing, but these molecules are disrupted in obesity.
- Despite functional delays, the liver’s molecular network remains structurally intact, suggesting potential for recovery.
Why This Matters
The liver plays a central role in metabolic adaptation, balancing energy distribution during starvation. While obesity slows down this response, the study confirms the network’s resilience—offering hope for future therapies targeting metabolic disorders.
Research Breakthrough
Led by Keigo Morita and Shinya Kuroda, the team analyzed time-series data from healthy and obese mice, overcoming a long-standing challenge in biology: tracking temporal changes in large-scale molecular networks.
“Molecules form a complex network, with hub molecules like ATP regulating metabolism,” explains Kuroda. “Obesity disrupts timing, not structure—meaning the system may still be fixable.”
Implications for Future Studies
The findings pave the way for deeper research into:
✔ Metabolic diseases (diabetes, fatty liver)
✔ Starvation adaptation
✔ Time-based biological modeling
Read the full study in Science Signaling.