Intermittent fasting has emerged as a popular approach to enhance health and boost metabolism. However, recent research indicates that its advantages may be diminished by body fat due to inconspicuous disruptions in the liver’s hunger adaptation.
In a study, researchers assessed liver modifications in both healthy and obese mice that lacked leptin, the hormone responsible for regulating appetite, during food deprivation periods. Intermittent fasting entails extended calorie restriction followed by a regular eating window.
Both mouse groups exhibited similar metabolic networks, comprising liver molecules that collaboratively manage energy; however, significant differences in timing were observed.
“In a healthy liver, energy-centric molecules such as adenosine triphosphate (ATP) and adenosine monophosphate (AMP) quickly respond to starvation and modulate various metabolic reactions,” stated Professor Shinya Kuroda in BBC Science Focus.
“This mechanism appears to be deficient and confused in obese individuals.”
To put it differently, in healthy mice, energy-related molecules like ATP and AMP operate as primary hubs, swiftly adapting metabolic responses to conserve and redistribute energy. Conversely, in obese mice, these molecules did not exhibit a quick response, resulting in a sluggish and disoriented reaction to starvation.
A rapid response from ATP and AMP during periods of food scarcity enables the liver to utilize energy from stored reserves. This process is believed to facilitate several benefits of intermittent fasting, such as weight reduction and better glycemic control.
Through a combination of structural and temporal metabolic analyses, the research team elucidates how obesity induces metabolic “jet lag,” complicating not just the timing but also the manner in which crucial molecular events transpire.
“Our findings could have significant implications for enhancing the effectiveness of intermittent fasting in humans,” Kuroda remarked.
“Next, we aim to identify easily detectable blood-based biomarkers in humans,” Kuroda added. “Ultimately, clinical research is necessary to assess our findings. The journey is lengthy, but every thousand-mile journey begins with a single step.”
This research was published in Science Signaling.
About Our Experts
Shinya Kuroda is a professor at the Faculty of Science at the University of Tokyo, Japan, focusing on Systems Biology. His research includes publications in Cell, Journal of Biochemistry, and Natural Cell Biology.
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Source: www.sciencefocus.com
