The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.
Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats
Open accessAbstract
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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In the citing paper
“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 the citing paper
“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 the citing paper
“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 the citing paper
“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 the citing paper
“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]
In the citing paper
“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 [7]
In the citing paper
“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 [16]
In the citing paper
“our studies and others showed that peripheral OXT delivery can work to exert anti-obesity effects [15], [16]”
From Treatment of obesity and diabetes using oxytocin or analogs in patients and mouse models (2013) · cites this paper as [16]
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Metadata
- 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
- Publisher
- American Physiological Society
- Published
- 2012-01-01
- Volume
- 302
- Issue
- 1
- Pages
- E134-E144
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- PMC
- PMC3328087
- 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
- green
- europepmc.org
- 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
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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