Dopamine Signaling in the Suprachiasmatic Nucleus Enables Weight Gain Associated with Hedonic Feeding
| Autor: | John N. Campbell, Aarti M. Purohit, Martin Wu, Anthony J. Spano, Jay Hirsh, Andrew D. Steele, Michael Scott, Sean R. Chadwick, Krystyna J. Cios, Michael Sidikpramana, Ali D. Güler, Qijun Tang, Christopher D. Deppmann, Yingnan Gao, Laura Sipe, Nidhi M. Purohit, Ryan M. Grippo, Meghana D. Sunkara, Qi Zhang, Everett Altherr |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Dopamine Gene Expression Nucleus accumbens Biology Weight Gain General Biochemistry Genetics and Molecular Biology Article Eating Mice Random Allocation 03 medical and health sciences 0302 clinical medicine Reward Orexigenic medicine Animals Circadian rhythm Overeating Suprachiasmatic nucleus Receptors Dopamine D1 Dopaminergic Feeding Behavior Mice Inbred C57BL 030104 developmental biology Dopamine receptor Suprachiasmatic Nucleus General Agricultural and Biological Sciences Neuroscience 030217 neurology & neurosurgery Signal Transduction medicine.drug |
| Zdroj: | Curr Biol |
| Popis: | Summary The widespread availability of energy-dense, rewarding foods is correlated with the increased incidence of obesity across the globe. Overeating during mealtimes and unscheduled snacking disrupts timed metabolic processes, which further contribute to weight gain. The neuronal mechanism by which the consumption of energy-dense food restructures the timing of feeding is poorly understood. Here, we demonstrate that dopaminergic signaling within the suprachiasmatic nucleus (SCN), the central circadian pacemaker, disrupts the timing of feeding, resulting in overconsumption of food. D1 dopamine receptor (Drd1)-null mice are resistant to diet-induced obesity, metabolic disease, and circadian disruption associated with energy-dense diets. Conversely, genetic rescue of Drd1 expression within the SCN restores diet-induced overconsumption, weight gain, and obesogenic symptoms. Access to rewarding food increases SCN dopamine turnover, and elevated Drd1-signaling decreases SCN neuronal activity, which we posit disinhibits downstream orexigenic responses. These findings define a connection between the reward and circadian pathways in the regulation of pathological calorie consumption. |
| Databáze: | OpenAIRE |
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