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Cited by 149Regulation of Appetite and ObesityNeuroendocrine regulation and behaviorNeuropeptides and Animal Physiology

The DOI matches its Crossref record; 108 of the 111 references it cites were found in a registry or an index.

Oxytocin, Feeding, and Satiety

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Sabatier, Nancy, Leng, Gareth, Menzies, John·2013·Frontiers in Endocrinology
DOI 10.3389/fendo.2013.00035PMC PMC3603288
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Abstract

Oxytocin neurons have a physiological role in food intake and energy balance. Central administration of oxytocin is powerfully anorexigenic, reducing food intake and meal duration. The central mechanisms underlying this effect of oxytocin have become better understood in the past few years. Parvocellular neurons of the paraventricular nucleus project to the caudal brainstem to regulate feeding via autonomic functions including the gastrointestinal vago-vagal reflex. In contrast, magnocellular neurons of the supraoptic and paraventricular nuclei release oxytocin from their dendrites to diffuse to distant hypothalamic targets involved in satiety. The ventromedial hypothalamus, for example, expresses a high density of oxytocin receptors but does not contain detectable oxytocin nerve fibers. Magnocellular neurons represent targets for the anorexigenic neuropeptide α-melanocyte stimulating hormone. In addition to homeostatic control, oxytocin may also have a role in reward-related feeding. Evidence suggests that oxytocin can selectively suppress sugar intake and that it may have a role in limiting the intake of palatable food by inhibiting the reward pathway.

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Crossref · 10.3389/fendo.2013.00035

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Figure 1 Responses to icv oxytocin in VMN neurons in vivo. Single VMN neurons were recorded extracellularly from the VMN of urethane-anesthetized rats (Sabatier and Leng, 2008). (A) Each bar represent the mean change in firing rate (±SD) averaged over the first 10 min after icv injection of oxytocin (1–10 ng) in each VMN cell tested. The cells are ranked by response magnitude and are classed as inhibited, non-responsive, and excited according to whether the responses were significant or not. (B) Representative example of an inhibition (left panel) and activation (right panel) of the mean firing rate in response to icv oxytocin in a single VMN cell recorded extracellularly. (C) Mean change in firing rate (±SE) in the VMN cells that were significantly activated ; n = 14), significantly inhibited ; n = 4), and not significantly affected ; n = 43) by icv oxytocin.
Figure 1 Responses to icv oxytocin in VMN neurons in vivo. Single VMN neurons were recorded extracellularly from the VMN of urethane-anesthetized rats (Sabatier and Leng, 2008). (A) Each bar represent the mean change in firing rate (±SD) averaged over the first 10 min after icv injection of oxytocin (1–10 ng) in each VMN cell tested. The cells are ranked by response magnitude and are classed as inhibited, non-responsive, and excited according to whether the responses were significant or not. (B) Representative example of an inhibition (left panel) and activation (right panel) of the mean firing rate in response to icv oxytocin in a single VMN cell recorded extracellularly. (C) Mean change in firing rate (±SE) in the VMN cells that were significantly activated ; n = 14), significantly inhibited ; n = 4), and not significantly affected ; n = 43) by icv oxytocin.CC BY · PubMed Central
Figure 2 Correlation of responses to icv oxytocin and iv CCK in VMN neurons in vivo. (A) Mean change in firing rate (±SE) in response to icv oxytocin (1–10 ng) in single VMN cells that were activated ; n = 5), inhibited ; n = 4), and not affected ; n = 6) by iv CCK injection. (B) Rank correlation of responses to CCK and oxytocin (high ranks excited; low ranks inhibited). The solid line is the linear fit to the ranks (r2 = 0.65). (C) Example of convergent responses to icv oxytocin (1–10 ng) and iv CCK (20 μg/kg) in a single VMN neuron.
Figure 2 Correlation of responses to icv oxytocin and iv CCK in VMN neurons in vivo. (A) Mean change in firing rate (±SE) in response to icv oxytocin (1–10 ng) in single VMN cells that were activated ; n = 5), inhibited ; n = 4), and not affected ; n = 6) by iv CCK injection. (B) Rank correlation of responses to CCK and oxytocin (high ranks excited; low ranks inhibited). The solid line is the linear fit to the ranks (r2 = 0.65). (C) Example of convergent responses to icv oxytocin (1–10 ng) and iv CCK (20 μg/kg) in a single VMN neuron.CC BY · PubMed Central
Figure 3 (A) Magnocellular oxytocin neurons are inhibited by icv injections of α-MSH and this effect can be blocked by pre-administration of a CB1 cannabinoid antagonist (Sabatier et al., 2003). (B) Oxytocin secretion from the posterior pituitary gland is reduced by icv injection of MC4 agonists. (C) However, α-MSH and MC4 agonists induce Fos expression in magnocellular oxytocin neurons and (D) induce dendritic oxytocin release. (E) Application of α-MSH retrodialysis to the SON affects the electrical activity of VMN neurons in vivo. Mean change in firing rate (±SE) in VMN neurons that were not affected (open bars; n = 13), and activated (solid bars; n = 8; P < 0.005, 0–30 min vs. control) in the 30 min period from the start of α-MSH infusion (100 μM) on the SON.
Figure 3 (A) Magnocellular oxytocin neurons are inhibited by icv injections of α-MSH and this effect can be blocked by pre-administration of a CB1 cannabinoid antagonist (Sabatier et al., 2003). (B) Oxytocin secretion from the posterior pituitary gland is reduced by icv injection of MC4 agonists. (C) However, α-MSH and MC4 agonists induce Fos expression in magnocellular oxytocin neurons and (D) induce dendritic oxytocin release. (E) Application of α-MSH retrodialysis to the SON affects the electrical activity of VMN neurons in vivo. Mean change in firing rate (±SE) in VMN neurons that were not affected (open bars; n = 13), and activated (solid bars; n = 8; P < 0.005, 0–30 min vs. control) in the 30 min period from the start of α-MSH infusion (100 μM) on the SON.CC BY · PubMed Central

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Metadata

Authors
Sabatier, N., Leng, G., & Menzies, J.
Affiliations
University of Edinburgh (GB)
Corresponding author
Menzies, John
ORCID
Venue
Frontiers in Endocrinology
Publisher
Frontiers Media SA
Published
2013
Volume
4
Pages
35-35
ISSN
1664-2392 (ISSN-L)
DOI
10.3389/fendo.2013.00035
PMC
PMC3603288
OpenAlex
W2131330949
Cited by
149
References
108
Citations by year
2026: 4 · 2025: 6 · 2024: 6 · 2023: 8 · 2022: 13 · 2021: 17 · 2020: 9 · 2019: 17 · 2018: 15 · 2017: 15 · 2016: 15 · 2015: 16 · 2014: 7 · 2013: 1
FWCI
7.02
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Endocrinology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, cc-by)
Funders
  • Medical Research Scotland
  • Biotechnology and Biological Sciences Research Council (BB/E015123/1)
  • FP7 Food, Agriculture and Fisheries, Biotechnology (266408, 245009)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
oxytocin, feeding behavior, satiety, anorectic effect, paraventricular nucleus, supraoptic nucleus, magnocellular neurons, parvocellular neurons, ventromedial hypothalamus, oxytocin receptor, alpha-melanocyte-stimulating hormone, energy balance, vago-vagal reflex, food reward, sugar consumption, palatable food intake

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