Cited by 439Regulation of Appetite and ObesitySmoking Behavior and CessationNicotinic Acetylcholine Receptors Study

Nicotine Decreases Food Intake Through Activation of POMC Neurons

Open access
Mineur, Yann S., Abizaid, Alfonso, Rao, Yan, Salas, Ramiro, DiLeone, Ralph J., Gündisch, Daniela, Diano, Sabrina, De Biasi, Mariella +3 more·2011·Science

Abstract

Nicotine decreases weight gain by targeting a brain pathway involved in the regulation of energy balance and food intake.

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Integrity signals

Registry

Crossref · 10.1126/science.1201889

Cites

35 of 35 references verified0 citation errors · 0 not checkable

Statistics

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  • Nicotine has appetite-suppressing effects, leading many smokers to report reduced food intake.

    “Nicotine, the primary psychoactive component of tobacco, is known to cause appetite-suppressing effects leading many smokers to report reduced food intake on one hand”

    From Smoking and its impact on eating behavior: A review (2026) · cites this paper as [6]

    The Abstract says smoking decreases appetite, and the paper reports that nicotine decreases food intake in mice. It also says smokers often report smoking to control their weight, but it does not say that many smokers report reduced food intake. (LLM, conf=0.83)

    Experimental — accuracy not yet measured
  • Nicotine interacts with the brain's reward system and alters neurotransmitter activity, particularly dopamine and serotonin, which play key roles in hunger and satiety regulation.

    “Studies have shown that nicotine interacts with the brain's reward system and alters neurotransmitter activity, particularly dopamine and serotonin, which play key roles in hunger and satiety regulation [2, 3, 4, 5-6].”

    From Smoking and its impact on eating behavior: A review (2026) · cites this paper as [6]

    The paper reports that nicotine activates hypothalamic POMC neurons through nicotinic acetylcholine receptors and decreases food intake in mice (Abstract; no page given). It does not establish the claimed reward-system mechanism or identify dopamine and serotonin as the neurotransmitters involved in hunger and satiety regulation; searches for those terms found no supporting passage. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Tobacco smokers usually have lower body weight and body mass index (BMI) compared to nonsmokers, which may be explained by the suppressive effect of nicotine on appetite.

    “Tobacco smokers usually have lower body weight and body mass index (BMI) compared to nonsmokers, which may be explained by the suppressive effect of nicotine on appetite [17].”
  • In vivo, nicotine increases c-fos immunoreactivity predominantly in POMC-positive cells.

    “and in vivo, as evidenced by an increase in c-fos immunoreactivity predominantly in POMC-positive cells (Huang et al., 2011; Mineur et al., 2011).”
  • The increase in POMC neuron activity predominates in vitro due to more rapid desensitization of nAChR responses in NPY neurons.

    “although the increase in POMC neuron activity predominates in vitro due to more rapid desensitization of nAChR responses in NPY neurons”

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Cites

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Research works printed but not linked: 1

  1. [15]Freeman ME Grattan DR Houpt TA Michael Conn P Neuroscience in Medicine 2008 301 358 Humana Press

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Authors
Mineur, Y. S., Abizaid, A., Rao, Y., Salas, R., DiLeone, R. J., Gündisch, D., Diano, S., De Biasi, M., Horvath, T. L., Gao, X.-B., & Picciotto, M. R.
Affiliations
  • Yale University (US)
  • Baylor College of Medicine (US)
  • University of Hawaii at Hilo (US)
  • Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.
  • Department of Comparative Medicine, Yale University School of Medicine, 34 Park Street, Third Floor Research, New Haven, CT 06508, USA.
Corresponding author
Picciotto, Marina R.
Venue
Science
Published
2011-06-10
Volume
332
Issue
6035
Pages
1330-1332
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2070076444
Cited by
439
References
35
Citations by year
2026: 16 · 2025: 22 · 2024: 47 · 2023: 18 · 2022: 24 · 2021: 26 · 2020: 22 · 2019: 31 · 2018: 31 · 2017: 32 · 2016: 24 · 2015: 27 · 2014: 31 · 2013: 32 · 2012: 38
FWCI
17.58
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (DP1OD006850)
  • National Institute on Alcohol Abuse and Alcoholism (P50AA015632, AA15632)
  • National Institute on Drug Abuse (DA14241, K02DA000436, DA017173, R01DA014241, R01DA017173, DA 00436, R37DA014241)
  • National Cancer Institute (U19CA148127)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK070723, DK-080000, DK-070039, DK 070723, R01DK070039, R01DK080000)
  • National Center for Research Resources (RR016467, P20RR016467)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
Keywords
nicotine, dietary intake, appetite, proopiomelanocortin neurons, melanocortin-4 receptor, nicotinic acetylcholine receptors, alpha3beta4 nicotinic receptor, hypothalamus, melanocortin system, body weight regulation, obesity
MeSH terms
Quinolizidine Alkaloids, Alkaloids, Animals, Azocines, Eating, Ganglionic Stimulants, Male, Mice, Inbred C57BL, Neurons, Nicotine, Pro-Opiomelanocortin, Quinolizines, Receptors, Nicotinic, Mice, Knockout, Nicotinic Agonists, Mice, Melanocortins

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