Abstract Title:

Sucralose Promotes Food Intake through NPY and a Neuronal Fasting Response.

Abstract Source:

Cell Metab. 2016 Jul 12 ;24(1):75-90. PMID: 27411010

Abstract Author(s):

Qiao-Ping Wang, Yong Qi Lin, Lei Zhang, Yana A Wilson, Lisa J Oyston, James Cotterell, Yue Qi, Thang M Khuong, Noman Bakhshi, Yoann Planchenault, Duncan T Browman, Man Tat Lau, Tiffany A Cole, Adam C N Wong, Stephen J Simpson, Adam R Cole, Josef M Penninger, Herbert Herzog, G Gregory Neely

Article Affiliation:

Qiao-Ping Wang


Non-nutritive sweeteners like sucralose are consumed by billions of people. While animal and human studies have demonstrated a link between synthetic sweetener consumption and metabolic dysregulation, the mechanisms responsible remain unknown. Here we use a diet supplemented with sucralose to investigate the long-term effects of sweet/energy imbalance. In flies, chronic sweet/energy imbalance promoted hyperactivity, insomnia, glucose intolerance, enhanced sweet taste perception, and a sustained increase in food and calories consumed, effects that are reversed upon sucralose removal. Mechanistically, this response was mapped to the ancient insulin, catecholamine, and NPF/NPY systems and the energy sensor AMPK, which together comprise a novel neuronal starvation response pathway. Interestingly, chronic sweet/energy imbalance promoted increased food intake in mammals as well, and this also occurs through an NPY-dependent mechanism. Together, our data show that chronic consumption of a sweet/energy imbalanced diet triggers a conserved neuronal fasting response and increases the motivation to eat.

Study Type : Animal Study

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