Cited by 214Regulation of Appetite and ObesityNeuroendocrine regulation and behaviorAdipokines, Inflammation, and Metabolic Diseases

Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats

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Morton, Gregory J., Thatcher, Brendan S., Reidelberger, Roger D., Ogimoto, Kayoko, Wolden-Hanson, Tami, Baskin, Denis G., Schwartz, Michael W., Blevins, James E.·2012·American Journal of Physiology-Endocrinology and Metabolism

Abstract

Growing evidence suggests that oxytocin plays an important role in the regulation of energy balance and that central oxytocin administration induces weight loss in diet-induced obese (DIO) animals. To gain a better understanding of how oxytocin mediates these effects, we examined feeding and neuronal responses to oxytocin in animals rendered obese following exposure to either a high-fat (HFD) or low-fat diet (LFD). Our findings demonstrate that peripheral administration of oxytocin dose-dependently reduces food intake and body weight to a similar extent in rats maintained on either diet. Moreover, the effect of oxytocin to induce weight loss remained intact in leptin receptor-deficient Koletsky (fa(k)/fa(k)) rats relative to their lean littermates. To determine whether systemically administered oxytocin activates hindbrain areas that regulate meal size, we measured neuronal c-Fos induction in the nucleus of the solitary tract (NTS) and area postrema (AP). We observed a robust neuronal response to oxytocin in these hindbrain areas that was unexpectedly increased in rats rendered obese on a HFD relative to lean, LFD-fed controls. Finally, we report that repeated daily peripheral administration of oxytocin in DIO animals elicited a sustained reduction of food intake and body weight while preventing the reduction of energy expenditure characteristic of weight-reduced animals. These findings extend recent evidence suggesting that oxytocin circumvents leptin resistance and induces weight-loss in DIO animals through a mechanism involving activation of neurons in the NTS and AP, key hindbrain areas for processing satiety-related inputs.

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Crossref · 10.1152/ajpendo.00296.2011

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  • In rodent studies, oxytocin affects energy expenditure.

    “evidence from rodent studies indicates that the neuropeptide acts as a strong inhibitor of food intake and affects energy expenditure and glucose homeostasis (6–9).”

    From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [7]

  • In rodent studies, oxytocin acts as a strong inhibitor of food intake.

    “evidence from rodent studies indicates that the neuropeptide acts as a strong inhibitor of food intake and affects energy expenditure and glucose homeostasis (6–9).”

    From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [7]

  • In rodent studies, oxytocin affects glucose homeostasis.

    “evidence from rodent studies indicates that the neuropeptide acts as a strong inhibitor of food intake and affects energy expenditure and glucose homeostasis (6–9).”

    From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [7]

  • Peripheral administration of high oxytocin doses can mimic the feeding-inhibitory effect, supposedly by triggering hypothalamic oxytocin release in a feed-forward fashion.

    “This effect could be mimicked by the peripheral administration of high oxytocin doses that supposedly trigger hypothalamic oxytocin release in a feed-forward fashion (7,12).”

    From Oxytocin Reduces Reward-Driven Food Intake in Humans (2013) · cites this paper as [7]

  • In another study of diet induced obesity in rats, systemic oxytocin reduced caloric intake and body weight without changing REE, indicating that oxytocin blocked the effect of weight loss to reduce energy expenditure.

    “In another study of diet induced obesity in rats, systemic oxytocin reduced caloric intake and body weight without changing REE, indicating that oxytocin blocked the effect of weight loss to reduce energy expenditure(33).”

    From Oxytocin reduces caloric intake in men (2015) · cites this paper as [33]

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Authors
Morton, G. J., Thatcher, B. S., Reidelberger, R. D., Ogimoto, K., Wolden-Hanson, T., Baskin, D. G., Schwartz, M. W., & Blevins, J. E.
Affiliations
  • University of Washington (US)
  • United States Department of Veterans Affairs (US)
  • Creighton University (US)
  • Office of Research and Development Medical Research Service, Veterans Affairs Puget Sound Health Care System, Department of Veterans Affairs Medical Center, Seattle, Washington;
Corresponding author
Morton, Gregory J.
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2012-01-01
Volume
302
Issue
1
Pages
E134-E144
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2154655754
Cited by
213
References
66
Citations by year
2026: 3 · 2025: 11 · 2024: 16 · 2023: 3 · 2022: 13 · 2021: 24 · 2020: 17 · 2019: 18 · 2018: 20 · 2017: 22 · 2016: 19 · 2015: 12 · 2014: 16 · 2013: 11 · 2012: 7
FWCI
5.17
Type
journal article
Language
en
Open access
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Washington
  • National Institutes of Health (1u24dk076126-01)
  • Nutrition Obesity Research Center, University of North Carolina
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-083042, DK-068304, U24-DK076126, P30-DK 17047, R01DK089056, DK089056, DK052989, R01DK052989, R01DK090320, P30DK035816, P30DK017047, R01DK083042)
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, diet-induced obesity, dietary intake, weight loss, energy balance, leptin resistance, leptin receptor deficiency, high-fat diet, nucleus tractus solitarius, area postrema, c-Fos neuronal activation, satiety, energy expenditure, hindbrain
MeSH terms
Animals, Appetite Depressants, Combined Modality Therapy, Crosses, Genetic, Dietary Fats, Dose-Response Relationship, Drug, Injections, Intraperitoneal, Male, Nerve Tissue Proteins, Neurons, Obesity, Oxytocin, Rats, Mutant Strains, Recombinant Proteins, Weight Loss, Proto-Oncogene Proteins c-fos, Rats, Sprague-Dawley, Solitary Nucleus, Leptin, Area Postrema, Rats, Receptors, Leptin

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