| Autor: |
Christina E. May, Anoumid Vaziri, Yong Qi Lin, Olga Grushko, Morteza Khabiri, Qiao-Ping Wang, Kristina J. Holme, Scott D. Pletcher, Peter L. Freddolino, G. Gregory Neely, Monica Dus |
| Jazyk: |
angličtina |
| Rok vydání: |
2019 |
| Předmět: |
|
| Zdroj: |
Cell Reports, Vol 27, Iss 6, Pp 1675-1685.e7 (2019) |
| Druh dokumentu: |
article |
| ISSN: |
2211-1247 |
| DOI: |
10.1016/j.celrep.2019.04.027 |
| Popis: |
Summary: Recent studies find that sugar tastes less intense to humans with obesity, but whether this sensory change is a cause or a consequence of obesity is unclear. To tackle this question, we study the effects of a high sugar diet on sweet taste sensation and feeding behavior in Drosophila melanogaster. On this diet, fruit flies have lower taste responses to sweet stimuli, overconsume food, and develop obesity. Excess dietary sugar, but not obesity or dietary sweetness alone, caused taste deficits and overeating via the cell-autonomous action of the sugar sensor O-linked N-Acetylglucosamine (O-GlcNAc) transferase (OGT) in the sweet-sensing neurons. Correcting taste deficits by manipulating the excitability of the sweet gustatory neurons or the levels of OGT protected animals from diet-induced obesity. Our work demonstrates that the reshaping of sweet taste sensation by excess dietary sugar drives obesity and highlights the role of glucose metabolism in neural activity and behavior. : May et al. discover that excess dietary sugar promotes overfeeding by dulling sweet taste sensation in Drosophila melanogaster. Deficits in taste function occur independently of obesity and, instead, develop because of higher glucose utilization inside the gustatory neurons. Correcting sweet taste function prevents overconsumption and obesity in animals fed a high sugar diet. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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