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Cell Metab. 2016 Jul 12;24(1):75-90. doi: 10.1016/j.cmet.2016.06.010.

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

Author information

1
Charles 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.
2
Neuroscience Division, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney, NSW 2010, Australia.
3
Charles Perkins Centre and School of Life and Environmental Sciences, The University of Sydney, Sydney, NSW 2006, Australia.
4
Sacred Heart College, Retreat Rd, Newtown, Geelong, Victoria 3220, Australia.
5
IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr. Bohr Gasse 3-5, A-1030 Vienna Austria.
6
Neuroscience Division, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney, NSW 2010, Australia. Electronic address: h.herzog@garvan.org.au.
7
Charles 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. Electronic address: greg.neely@sydney.edu.au.

Abstract

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.

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PMID:
27411010
DOI:
10.1016/j.cmet.2016.06.010
[Indexed for MEDLINE]
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