التفاصيل البيبلوغرافية
| العنوان: |
Dopamine production in neurotensin receptor 1 neurons is required for diet‐induced obesity and increased day eating on a high‐fat diet. |
| المؤلفون: |
Farahmand, Firozeh, Sidikpramana, Michael, Gomez, Alyssa R., Rivera, Luis J., Trzeciak, Jacqueline R., Sharif, Sarah, Tang, Qijun, Leinninger, Gina M., Güler, Ali D., Steele, Andrew D. |
| المصدر: |
Obesity (19307381); Aug2024, Vol. 32 Issue 8, p1448-1452, 5p |
| مصطلحات موضوعية: |
HIGH-fat diet, DOPAMINERGIC neurons, NEUROTENSIN, DIETARY patterns, TYROSINE hydroxylase, DOPAMINE receptors |
| مستخلص: |
Objective: This study aimed to determine a dopaminergic circuit required for diet‐induced obesity in mice. Methods: We created conditional deletion mutants for tyrosine hydroxylase (TH) using neurotensin receptor 1 (Ntsr1) Cre and other Cre drivers and measured feeding and body weight on standard and high‐fat diets. We then used an adeno‐associated virus to selectively restore TH to the ventral tegmental area (VTA) Ntsr1 neurons in conditional knockout (cKO) mice. Results: Mice with cKO of Th using Vglut2‐Cre, Cck‐Cre, Calb1‐Cre, and Bdnf‐Cre were susceptible to obesity on a high‐fat diet; however, Ntsr1‐CreTh cKO mice resisted weight gain on a high‐fat diet and did not experience an increase in day eating unlike their wild‐type littermate controls. Restoration of TH to the VTA Ntsr1 neurons of the Ntsr1‐CreTh cKO mice using an adeno‐associated virus resulted in an increase in weight gain and day eating on a high‐fat diet. Conclusions: Ntsr1‐CreTh cKO mice failed to increase day eating on a high‐fat diet, offering a possible explanation for their resistance to diet‐induced obesity. These results implicate VTA Ntsr1 dopamine neurons as promoting out‐of‐phase feeding behavior on a high‐fat diet that could be an important contributor to diet‐induced obesity in humans. [ABSTRACT FROM AUTHOR] |
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