Cited by 235Regulation of Appetite and ObesityNeuroendocrine regulation and behaviorAdipokines, Inflammation, and Metabolic Diseases

Low sympathetic tone and obese phenotype in oxytocin-deficient mice

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Camerino, Claudia·2009·Obesity

Abstract

Oxytocin (Oxt) is secreted both peripherally and centrally and is involved in several functions including parturition, milk let-down reflex, social behavior, and food intake. Recently, it has been shown that mice deficient in Oxt receptor develop late-onset obesity. In this study, we characterized a murin model deficient in Oxt peptide (Oxt(-/-)) to evaluate food intake and body weight, glucose tolerance and insulin tolerance, leptin and adrenaline levels. We found that Oxt(-/-) mice develop late-onset obesity and hyperleptinemia without any alterations in food intake in addition to having a decreased insulin sensitivity and glucose intolerance. The lack of Oxt in our murin model also results in lower adrenalin levels which led us to hypothesize that the metabolic changes observed are associated with a decreased sympathetic nervous tone. It has been shown that Oxt neurons in the paraventricular nucleus (PVN) are a component of a leptin-sensitive signaling circuit between the hypothalamus and caudal brain stem for the regulation of food intake and energy homeostasis. Nevertheless, the lack of Oxt in these mice does not have a direct impact on feeding behavior whose regulation is probably dependent on the complex interplay of several factors. The lack of hyperphagia evident in the Oxt(-/-) mice may, in part, be attributed to the developmental compensation of other satiety factors such as cholecystokinin or bombesin-related peptides which merits further investigation. These findings identify Oxt as an important central regulator of energy homeostasis.

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  • Oxytocin and oxytocin receptor knockout mice develop late-onset obesity in the absence of hyperphagia.

    “These mice develop late-onset obesity in the absence of hyperphagia (65, 66).”
  • Preclinical research indicates that oxytocin may be involved in glucose homeostasis.

    “Preclinical research indicates that oxytocin may be involved in glucose homeostasis.”

    From Oxytocin reduces caloric intake in men (2015) · cites this paper as [38]

  • Oxytocin knockout mice develop insulin resistance and glucose intolerance.

    “Oxytocin knockout mice develop insulin resistance and glucose intolerance(38).”

    From Oxytocin reduces caloric intake in men (2015) · cites this paper as [38]

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  1. Kronenberg H, Melmed S, Polonsky KS, Larsen PR. Williams Textbook of Endocrinology. Saunders Elseviers: Amsterdam, the Netherlands, 2007.

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Authors
Camerino, C.
Affiliations
University of Bari Aldo Moro (IT)
Corresponding author
Camerino, Claudia
Venue
Obesity
Publisher
Wiley
Published
2009-05
Volume
17
Issue
5
Pages
980-984
ISSN
  • 1930-7381 (ISSN-L)
  • 1930-739X
OpenAlex
W2013694191
Cited by
235
References
26
Citations by year
2026: 8 · 2025: 9 · 2024: 24 · 2023: 11 · 2022: 9 · 2021: 17 · 2020: 10 · 2019: 15 · 2018: 19 · 2017: 18 · 2016: 17 · 2015: 16 · 2014: 18 · 2013: 12 · 2012: 13
FWCI
4.79
Type
journal article
Language
en
Open access
Locations
  • Obesity (publishedVersion)
  • PubMed (publishedVersion)
  • CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
oxytocin, late-onset obesity, hyperleptinemia, insulin resistance, impaired glucose tolerance, epinephrine, paraventricular nucleus, energy homeostasis, dietary intake, leptin, cholecystokinin, bombesin, satiety peptides
MeSH terms
Adipose Tissue, Animals, Blood Glucose, Body Weight, Brain Stem, Energy Intake, Crosses, Genetic, Hypothalamus, Insulin, Mice, Inbred C57BL, Obesity, Oxytocin, Stomach, Sympathetic Nervous System, Signal Transduction, Glucose Intolerance, Mice, Knockout, Leptin, Mice

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