ArticleMolecular metabolism2014
The reward value of sucrose in leptin-deficient obese mice.
Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- The leptin fragment Lep116-130 attenuates hedonic consumption and sucrose-seeking in mice.Frontiers in pharmacology · 2026Article
- Dysregulation of FGFR1 signaling in the hippocampus facilitates depressive disorder.Experimental & molecular medicine · 2025Article
- Insects as a New Complex Model in Hormonal Basis of Obesity.International journal of molecular sciences · 2021Review
- Effect of short-term intake of four sweeteners on feed intake, solution consumption and neurotransmitters release on mice.Journal of food science and technology · 2021Article
- Nesfatin-1 decreases the motivational and rewarding value of food.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- The LepR-mediated leptin transport across brain barriers controls food reward.Molecular metabolism · 2018Article
- Flavor preferences conditioned by nutritive and non-nutritive sweeteners in mice.Physiology & behavior · 2017Article
- A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila.Cell metabolism · 2017Article
- Article
- Decreased consumption of rewarding sucrose solutions after injection of melanocortins into the ventral tegmental area of rats.Psychopharmacology · 2015Article
- The emerging neurobiology of calorie addiction.eLife · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leptin-deficient patients report higher "liking" ratings for food, and leptin replacement therapy normalizes these ratings even before weight loss is achieved. Since animals cannot report their ratings, we studied the relationship between leptin and food reward in leptin-deficient ob/ob mice using a optogenetic assay that quantifies the reward value of sucrose. In this assay, mice chose between one sipper dispensing the artificial sweetener sucralose coupled to optogenetic activation of dopaminergic (DA) neurons, and another sipper dispensing sucrose. We found that the reward value of sucrose was high under a state of leptin deficiency, as well as at a dose of leptin that does not suppress food intake (12.5 ng/h). Treatment with higher doses of leptin decreased the reward value of sucrose before weight loss was achieved (100 ng/h), as seen in leptin-deficient patients. These results phenocopy in mice the behavior of leptin-deficient patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.