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Cited by 55Regulation of Appetite and ObesityNeuropeptides and Animal PhysiologyNeurotransmitter Receptor Influence on Behavior

Diet-induced obesity increases μ opioid receptor binding in specific regions of the rat brain

Smith, Sharon L, Harrold, Joanne A, Williams, Gareth·2002·Brain Research
DOI 10.1016/s0006-8993(02)03291-2
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Abstract

Mu (mu) opioid agonists preferentially increase the intake of highly palatable food. Here we investigated changes in mu opioid binding in feeding- and reward-related brain regions in rats given a palatable diet for 17 weeks. Diet feeding induced variable obesity, and rats were stratified into 'high-weight gain' (HWG: weight increase, 513-695 g; n=12) and 'low-weight gain' (LWG: range: 396-502 g; n=11) groups. Chow-fed controls (n=9) gained 324-487 g during this time. Body fat mass and plasma leptin and insulin were significantly higher in LWG than in controls and even higher in HWG. mu-Receptor binding (measured in brain slices using [3H]-DAMGO (D-Ala(2), N-Me-Phe(4),Gly-ol(5)) and quantitative autoradiography) was significantly increased in specific forebrain regions of diet-fed rats. In the fundus striati, dorsal endopiriform nucleus and medial preoptic area (MPA), binding was similarly increased (30-40%; P<0.05 vs. controls) in the HWG and LWG groups. Increases in mu binding paralleled weight gain in the basolateral amygdala and basomedial amygdala, being approximately 20% above controls (P<0.001) in LWG and approximately 30% higher in HWG (P<0.05 vs. LWG). The medial habenula showed significantly higher binding (by approximately 40%) in HWG, with no significant changes in LWG. In all these areas (except the MPA), binding was significantly correlated with plasma leptin and insulin. We suggest that increased mu binding reflects decreased release of endogenous mu opioid peptides. This orexigenic system therefore seems unlikely to drive appetite for palatable food. Indeed, the mu opioid system in reward-related areas may be inhibited in dietary obesity, probably by increased plasma leptin and insulin, and this may represent a failed homeostatic attempt to limit overeating and eventually obesity.

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Crossref · 10.1016/s0006-8993(02)03291-2

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  • A highly palatable food diet can induce obesity in rats, with weight increases correlating with increases in m-opioid peptide binding in the basolateral and basomedial amygdala.

    “A highly palatable food diet can induce obesity in rats, with the weight increases correlating with increases in m-opioid peptide binding in the basolateral and basomedial amygdala.”

    From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [157]

  • The medial habenula showed significantly higher m-opioid peptide binding (by approximately 40%) after exposure to the palatable food in the rats that gained weight (those that consumed more food) but not in those that did not.

    “Interestingly, the medial habenula showed significantly higher m-opioid peptide binding (by approximately 40%) after exposure to the palatable food in the rats that gained weight (those that consumed more food) but not in those that did not (157).”

    From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [157]

  • The medial habenula showed significantly higher μ-opioid peptide binding (by approximately 40%) after exposure to the palatable food in the rats that gained weight but not in those that did not.

    “the medial habenula showed significantly higher µ-opioid peptide binding (by approximately 40%) after exposure to the palatable food in the rats that gained weight (those that consumed more food) but not in those that did not (Smith et al 2002)”

    From Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction (2011) · cites this paper as Smith et al 2002

  • A highly palatable food diet can induce obesity in rats, with the weight increases correlating with increases in μ-opioid peptide binding in the basolateral and basomedial amygdala.

    “A highly palatable food diet can induce obesity in rats, with the weight increases correlating with increases in µ-opioid peptide binding in the basolateral and basomedial amygdala.”

    From Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction (2011) · cites this paper as Smith et al 2002

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Authors
Smith, S. L., Harrold, J. A., & Williams, G.
Affiliations
University of Liverpool (GB)
Corresponding author
Harrold, Joanne A
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2002-10
Volume
953
Issue
1-2
Pages
215-222
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/s0006-8993(02)03291-2
OpenAlex
W2064699474
Cited by
55
References
43
Citations by year
2025: 1 · 2023: 2 · 2022: 1 · 2020: 4 · 2019: 4 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 6 · 2014: 3 · 2013: 2 · 2012: 3
FWCI
1.16
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • Explore Bristol Research (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
mu-opioid receptor, diet-induced obesity, palatable diet, food reward, leptin, insulin, medial preoptic area, amygdala, medial habenula, endopiriform nucleus, striatum, endogenous opioids, appetite regulation, overeating
MeSH terms
Analgesics, Opioid, Animals, Appetite, Autoradiography, Brain, Diet, Insulin, Male, Obesity, Radioligand Assay, Reward, Rats, Wistar, Receptors, Opioid, mu, Leptin, Enkephalin, Ala(2)-MePhe(4)-Gly(5)-, Rats

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