Sucralose Promotes Food Intake through NPY and a Neuronal Fasting Response.
Qiao-Ping Wang1, Yong Qi Lin1, Lei Zhang2
1Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW 2006, Australia; Neuroscience Division, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney, NSW 2010, Australia.
Artificial sweeteners like sucralose disrupt metabolism by triggering a conserved neuronal fasting response. This leads to increased food intake and hyperactivity, effects reversed upon sweetener removal.
Area of Science:
- Neuroscience
- Metabolic Science
- Animal Models
Background:
- Non-nutritive sweeteners (NNS) are widely consumed globally.
- Studies suggest a link between NNS and metabolic dysfunction, but mechanisms are unclear.
Purpose of the Study:
- Investigate long-term effects of sucralose-induced sweet/energy imbalance.
- Elucidate the neurobiological mechanisms underlying metabolic dysregulation from NNS.
Main Methods:
- Dietary sucralose supplementation in Drosophila melanogaster (fruit flies).
- Analysis of behavioral, metabolic, and neural pathways.
- Mammalian models to assess conserved mechanisms.
Main Results:
- In flies, chronic sucralose intake caused hyperactivity, insomnia, glucose intolerance, and increased appetite.
- These effects were reversed upon sucralose withdrawal.
- Mechanisms involved insulin, catecholamine, NPF/NPY systems, and AMPK, forming a novel starvation response pathway.
- Mammals also showed increased food intake via an NPY-dependent pathway.
Conclusions:
- Chronic consumption of sweet/energy imbalanced diets triggers conserved neuronal fasting responses.
- This pathway increases food intake motivation and contributes to metabolic dysregulation.
- Findings highlight potential risks of widespread NNS consumption.
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