ArticleObesity (Silver Spring, Md.)2024
Dopamine production in neurotensin receptor 1 neurons is required for diet-induced obesity and increased day eating on a high-fat diet.
Article in Obesity (Silver Spring, Md.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A population of dopaminergic neurons in the substantia nigra is required for food-anticipatory activity.Current biology : CB · 2026Article
- Beyond Pleasure: Unraveling the Multifaceted Role of Dopamine in Obesity and Metabolic Regulation.Current obesity reports · 2026Review
- Nmur1 and Cckar fail to support functional genetic access in adult dopamine neurons and challenge GPCR atlas assignments.bioRxiv : the preprint server for biology · 2026Article
- Genetic Identification of Dopamine Neurons Required for Circadian Food Anticipatory Activity in Mice.bioRxiv : the preprint server for biology · 2026Article
- CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice.Translational psychiatry · 2026Article
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Influence of the neurotensin signaling system on feeding and satiety.Neuropharmacology · 2025Review
- Overexpression of the short isoform of the dopamine D2 receptor causes diet-induced obesity and hyperglycemia in mice.Journal of neuroendocrinology · 2025Article
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Authors and funding
10 authors.
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Abstract
objectiveThis study aimed to determine a dopaminergic circuit required for diet-induced obesity in mice.
methodsWe 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.
resultsMice 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-Cre Th 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-Cre Th cKO mice using an adeno-associated virus resulted in an increase in weight gain and day eating on a high-fat diet.
conclusionsNtsr1-Cre Th 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.
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