Mechanisms of the anti-obesity effects of oxytocin in diet-induced obese rats
Open accessAbstract
Apart from its role during labor and lactation, oxytocin is involved in several other functions. Interestingly, oxytocin- and oxytocin receptor-deficient mice develop late-onset obesity with normal food intake, suggesting that the hormone might exert a series of beneficial metabolic effects. This was recently confirmed by data showing that central oxytocin infusion causes weight loss in diet-induced obese mice. The aim of the present study was to unravel the mechanisms underlying such beneficial effects of oxytocin. Chronic central oxytocin infusion was carried out in high fat diet-induced obese rats. Its impact on body weight, lipid metabolism and insulin sensitivity was determined. We observed a dose-dependent decrease in body weight gain, increased adipose tissue lipolysis and fatty acid β-oxidation, as well as reduced glucose intolerance and insulin resistance. The additional observation that plasma oxytocin levels increased upon central infusion suggested that the hormone might affect adipose tissue metabolism by direct action. This was demonstrated using in vitro, ex vivo, as well as in vivo experiments. With regard to its mechanism of action in adipose tissue, oxytocin increased the expression of stearoyl-coenzyme A desaturase 1, as well as the tissue content of the phospholipid precursor, N-oleoyl-phosphatidylethanolamine, the biosynthetic precursor of the oleic acid-derived PPAR-alpha activator, oleoylethanolamide. Because PPAR-alpha regulates fatty acid β-oxidation, we hypothesized that this transcription factor might mediate the oxytocin effects. This was substantiated by the observation that, in contrast to its effects in wild-type mice, oxytocin infusion failed to induce weight loss and fat oxidation in PPAR-alpha-deficient animals. Altogether, these results suggest that oxytocin administration could represent a promising therapeutic approach for the treatment of human obesity and type 2 diabetes.
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Oxytocin promotes energy expenditure.
“These studies suggest that oxytocin promotes energy expenditure.”
From Oxytocin reduces caloric intake in men (2015) · cites this paper as [7]
Oxytocin induces weight loss in rodents, and this effect may be related to increased energy expenditure and lipolysis in addition to appetite suppression.
“Oxytocin induces weight loss in rodents, and this effect may be related to increased energy expenditure and lipolyis in addition to appetite suppression(6, 7, 8, 9, 10, 11).”
From Oxytocin reduces caloric intake in men (2015) · cites this paper as [7]
In vitro and in vivo experiments have demonstrated that oxytocin inhibits adipogenesis and promotes lipolytic pathways and fatty acid oxidation.
“In vitro and in vivo experiments have demonstrated that oxytocin inhibits adipogenesis and promotes lipolytic pathways and fatty acid oxidation(7, 37).”
From Oxytocin reduces caloric intake in men (2015) · cites this paper as [7]
In an investigation of rats receiving a high fat diet, central oxytocin attenuated weight gain without changing food intake.
“In an investigation of rats receiving a high fat diet, central oxytocin attenuated weight gain without changing food intake(7).”
From Oxytocin reduces caloric intake in men (2015) · cites this paper as [7]
Oxytocin enhances insulin sensitivity and glucose tolerance in a rodent model of diet-induced obesity independent of its effects on body weight.
“Although this conclusion is in need of corroboration in experiments focusing on glucose homeostasis, it is in line with findings that oxytocin enhances insulin sensitivity and glucose tolerance in a rodent model of diet-induced obesity independent of its effects on body weight (7,50).”
From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [50]
Similar anti-obesity effects of OXT occur in rat models.
“similar anti-obesity effects of OXT were reported to occur in rat models [16], [17].”
From Treatment of obesity and diabetes using oxytocin or analogs in patients and mouse models (2013) · cites this paper as [17]
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- Authors
- Deblon, N., Veyrat-Durebex, C., Bourgoin, L., Caillon, A., Bussier, A.-L., Petrosino, S., Piscitelli, F., Legros, J.-J., Geenen, V., Foti, M., Wahli, W., Di Marzo, V., & Rohner-Jeanrenaud, F.
- Affiliations
- University of Geneva (CH)
- Istituto di Chimica Biomolecolare (IT)
- University of Liège (BE)
- University of Lausanne (CH)
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-09-27
- Volume
- 6
- Issue
- 9
- Pages
- e25565
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3181274
- OpenAlex
- W2161253360
- Cited by
- 254
- References
- 42
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 20 · 2023: 12 · 2022: 18 · 2021: 25 · 2020: 16 · 2019: 23 · 2018: 22 · 2017: 22 · 2016: 19 · 2015: 17 · 2014: 20 · 2013: 16 · 2012: 5
- FWCI
- 6.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
- IRIS (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Open Repository and Bibliography (University of Liège) (submittedVersion, other-oa)
- SERVAL (Université de Lausanne) (submittedVersion, other-oa)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- National Science Foundation (310030)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (120147, 128660, 135727, 31003A, 31003A-134919/1, 134919, 310000, 310030, 3100A0)
- National Institutes of Health (DA009789)
- National Institute on Drug Abuse (P01DA009789)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- oxytocin, anti-obesity, diet-induced obesity, high-fat diet, adipose tissue lipolysis, fatty acid beta-oxidation, insulin resistance, impaired glucose tolerance, PPARα, stearoyl-CoA desaturase 1, oleoylethanolamide, type 2 diabetes
- MeSH terms
- Adipose Tissue, Animals, Body Weight, Diet, Dose-Response Relationship, Drug, Insulin Resistance, Male, Obesity, Oleic Acids, Oxytocin, Anti-Obesity Agents, PPAR alpha, Mice, Rats, Gene Knockout Techniques, Endocannabinoids
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