Cited by 164Regulation of Appetite and ObesitySmoking Behavior and CessationAdipose Tissue and Metabolism

Effect of Short-Term Cigarette Smoke Exposure on Body Weight, Appetite and Brain Neuropeptide Y in Mice

Chen, Hui, Vlahos, Ross, Bozinovski, Steve, Jones, Jessica, Anderson, Gary P, Morris, Margaret J·2005·Neuropsychopharmacology

Abstract

Although nicotinic receptors have been demonstrated in hypothalamic appetite-regulating areas and nicotine administration alters food intake and body weight in both animals and humans, the mechanisms underlying the effects of smoking on appetite circuits remain unclear. Conflicting effects of nicotine on the major orexigenic peptide, neuropeptide Y (NPY), have been observed in the brain, but the effects of smoking are unknown. Thus, we aimed to investigate how cigarette smoking affects body weight, food intake, plasma leptin concentration, hypothalamic NPY peptide, adipose mass and mRNA expression of uncoupling proteins (UCP), and tumor necrosis factor (TNF) alpha. Balb/C mice (8 weeks) were exposed to cigarette smoke (three cigarettes, three times a day for 4 consecutive days) or sham exposed. Body weight and food intake were recorded. Plasma leptin and brain NPY were measured by radioimmunoassay. UCPs and TNF alpha mRNA were measured by real-time PCR. Food intake dropped significantly from the first day of smoking, and weight loss became evident within 2 days. Brown fat and retroperitoneal white fat masses were significantly reduced, and plasma leptin concentration was decreased by 34%, in line with the decreased fat mass. NPY concentrations in hypothalamic subregions were similar between two groups. UCP1 mRNA was decreased in white fat and UCP3 mRNA increased in brown fat in smoking group. Short-term cigarette smoke exposure led to reduced body weight, food intake, and fat mass. The reduction in plasma leptin concentration may have been too modest to increase NPY production; alternatively, change in NPY or its function might have been offset by nicotine or other elements in cigarette smoke.

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Crossref · 10.1038/sj.npp.1300597

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Authors
Chen, H., Vlahos, R., Bozinovski, S., Jones, J., Anderson, G. P., & Morris, M. J.
Affiliations
  • The University of Melbourne (AU)
  • The Royal Melbourne Hospital (AU)
Corresponding author
Morris, Margaret J
Venue
Neuropsychopharmacology
Published
2004-10-27
Volume
30
Issue
4
Pages
713-719
ISSN
  • 0893-133X (ISSN-L)
  • 1740-634X
OpenAlex
W2037326512
Cited by
164
References
62
Citations by year
2026: 1 · 2025: 3 · 2024: 8 · 2023: 3 · 2022: 11 · 2021: 7 · 2020: 8 · 2019: 7 · 2018: 8 · 2017: 6 · 2016: 9 · 2015: 11 · 2014: 10 · 2013: 7 · 2012: 9
FWCI
1.48
Type
journal article
Language
en
Open access
closed
Locations
  • Neuropsychopharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • UTS ePRESS (University of Technology Sydney) (submittedVersion)
Funders
  • Medical Research Council
  • National Health and Medical Research Council
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords
cigarette smoke exposure, nicotine, neuropeptide Y, appetite, dietary intake, body weight, leptin, hypothalamus, brown adipose tissue, white adipose tissue, uncoupling proteins, UCP1, UCP3, TNF-α, fat mass
MeSH terms
Uncoupling Protein 3, Uncoupling Protein 1, Adipose Tissue, Animals, Appetite Regulation, Body Weight, Brain, Carrier Proteins, Disease Models, Animal, Drug Administration Schedule, Energy Metabolism, Hypothalamus, Ion Channels, Male, Membrane Proteins, Mice, Inbred BALB C, Neuropeptide Y, Nicotine, RNA, Messenger, Smoking, Time Factors, Tobacco Use Disorder, Tumor Necrosis Factor-alpha, Down-Regulation, Leptin, Mitochondrial Proteins, Mice

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