Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice
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Leptin is a circulating protein involved in the long-term regulation of food intake and body weight. Cholecystokinin (CCK) is released postprandially and elicits satiety signals. We investigated the interaction between leptin and CCK-8 in the short-term regulation of food intake induced by 24-hr fasting in lean mice. Leptin, injected intraperitoneally (i.p.) at low doses (4–120 μg/kg), which did not influence feeding behavior for the first 3 hr postinjection, decreased food intake dose dependently by 47–83% during the first hour when coinjected with a subthreshold dose of CCK. Such an interaction was not observed between leptin and bombesin. The food-reducing effect of leptin injected with CCK was not associated with alterations in gastric emptying or locomotor behavior. Leptin–CCK action was blocked by systemic capsaicin at a dose inducing functional ablation of sensory afferent fibers and by devazepide, a CCK-A receptor antagonist but not by the CCK-B receptor antagonist, L-365,260. The decrease in food intake which occurs 5 hr after i.p. injection of leptin alone was also blunted by devazepide. Coinjection of leptin and CCK enhanced the number of Fos-positive cells in the hypothalamic paraventricular nucleus by 60%, whereas leptin or CCK alone did not modify Fos expression. These results indicate the existence of a functional synergistic interaction between leptin and CCK leading to early suppression of food intake which involves CCK-A receptors and capsaicin-sensitive afferent fibers.
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Circulating leptin changes rapidly in response to acute caloric intake or restriction, assisting in the control of short-term feeding via mechanisms such as augmentation of the anorectic effects of cholecystokinin.
“Circulating leptin changes rapidly in response to acute caloric intake or restriction, assisting in the control of short-term feeding via mechanisms such as augmentation of the anorectic effects of cholecystokinin, [57][58][59]”
From The effects of sleep disruption on metabolism, hunger, and satiety, and the influence of psychosocial stress and exercise: A narrative review (2024) · cites this paper as [59]
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OGAWA, R., STRADER, A., CLEGG, D., SAKAI, R., SEELEY, R., & WOODS, S. (2005) · Physiology & Behavior · doi:10.1016/j.physbeh.2005.08.028 · Cited by 15 · see citing works
Fortin, S. M., Chen, J., & Hayes, M. R. (2020) · Physiology & Behavior · doi:10.1016/j.physbeh.2020.112870 · Cited by 10 · see citing works
- Authors
- Barrachina, M. D., Martínez, V., Wang, L., Wei, J. Y., & Taché, Y.
- Affiliations
- University of California, Los Angeles (US)
- CURE: Digestive Diseases Research Center, West Los Angeles Veterans Affairs Medical Center, Department of Medicine, and Brain Research Institute, University of California, Los Angeles, CA 90073
- Salk Institute for Biological Studies (US)
- Corresponding author
- Taché, Yvette
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1997-09-16
- Volume
- 94
- Issue
- 19
- Pages
- 10455-10460
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC23384
- OpenAlex
- W1996634799
- Cited by
- 440
- References
- 73
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 1 · 2023: 5 · 2022: 7 · 2021: 13 · 2020: 9 · 2019: 9 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 10 · 2014: 25 · 2013: 12 · 2012: 18
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- National Institutes of Health (5r01dk030110-16, 5k05mh000663-07)
- National Institute of Mental Health (MH 00663)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 41301, DK30110, P30DK041301)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- leptin, cholecystokinin, CCK-8, food intake regulation, satiety, synergistic interaction, CCK-A receptor, bombesin, paraventricular nucleus, Fos expression, fasting, lean mice, hypothalamus
- MeSH terms
- Animals, Benzodiazepinones, Bombesin, Capsaicin, Cholecystokinin, Drug Synergism, Feeding Behavior, Gastric Emptying, Immunohistochemistry, Mice, Inbred C57BL, Motor Activity, Paraventricular Hypothalamic Nucleus, Proteins, Stereotyped Behavior, Devazepide, Leptin, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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