Cited by 68Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismPeroxisome Proliferator-Activated Receptors

Subchronic treatment of rats with oxytocin results in improved adipocyte differentiation and increased gene expression of factors involved in adipogenesis

Open access
Eckertova, Miroslava, Ondrejcakova, Maria, Krskova, Katarina, Zorad, Stefan, Jezova, Daniela·2011·British Journal of Pharmacology

Abstract

BACKGROUND AND PURPOSE: Treatment with thiazolidinediones, insulin-sensitizing drugs, enhances adipogenesis, which may result in unwanted increase in adiposity. Based on the suggested metabolic effects of oxytocin, the aims of the present study were to: (i) determine whether chronic treatment with oxytocin exerts positive effects on white adipose tissue growth without increasing adiposity; (ii) investigate possible mechanisms of action of oxytocin by measuring the level of gene expression of adipogenic factors; and (iii) test the hypothesis that oxytocin's effect on adipose tissue involves specific activation of eukaryotic elongation factor 2 (eEF2). EXPERIMENTAL APPROACH: Adult rats were subcutaneously treated with oxytocin (3.6 µg·100 g⁻¹ body weight day⁻¹) via osmotic minipumps for 2 weeks. Adipocytes from epididymal adipose tissue were isolated and their size evaluated by light microscopy. Gene expression of adipogenic and angiogenic factors was determined by real-time PCR and dephosphorylation of eEF2 by immunoblotting. KEY RESULTS: Oxytocin treatment decreased the diameter of adipocytes and increased the epididymal adipose tissue protein content without changing the adipose tissue mass. Increases in fatty acid binding protein, peroxisome proliferator-activated receptor γ, insulin-sensitive glucose transporter 4, leptin and CD31 mRNA levels were noted in the epididymal and/or retroperitoneal fat tissue of oxytocin-treated rats. Oxytocin enhanced the dephosphorylation of eEF2 in the epididymal adipose tissue. CONCLUSIONS AND IMPLICATIONS: The present results demonstrate that subchronic treatment with oxytocin induces adipogenic and angiogenic effects and that the eEF2 signalling pathway is involved in these effects of oxytocin on adipose tissue in vivo. These findings are likely to motivate further research and indicate new approaches for modulating adipose tissue morphology and metabolism.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/j.1476-5381.2010.01037.x

Cites

51 of 51 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Peripheral oxytocin administration in rats increases insulin-sensitive glucose transporter 4 mRNA in fat, suggesting a mechanism for increasing insulin sensitivity.

    “Peripheral oxytocin administration in rats increases insulin-sensitive glucose transporter 4 mRNA in fat, suggesting a mechanism for increasing insulin sensitivity(39).”

    From Oxytocin reduces caloric intake in men (2015) · cites this paper as [39]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Eckertova, M., Ondrejcakova, M., Krskova, K., Zorad, S., & Jezova, D.
Venue
British Journal of Pharmacology
Publisher
Wiley
Published
2010-12-14
Volume
162
Issue
2
Pages
452-463
ISSN
  • 0007-1188 (ISSN-L)
  • 1476-5381
OpenAlex
W1522228430
Cited by
68
References
51
Citations by year
2026: 2 · 2025: 3 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 8 · 2018: 6 · 2017: 5 · 2016: 5 · 2015: 6 · 2014: 4 · 2013: 5 · 2012: 2
FWCI
2.33
Type
journal article
Language
en
Open access
Locations
  • British Journal of Pharmacology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Vedecká Grantová Agentúra MŠVVaŠ SR a SAV
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
oxytocin, adipogenesis, white adipose tissue, elongation factor 2, PPARγ, fatty acid binding protein, glucose transporter 4, leptin, CD31, angiogenesis, epididymal adipose tissue, retroperitoneal fat, adiposity, thiazolidinediones
MeSH terms
Animals, Drug Evaluation, Preclinical, Male, Oxytocin, RNA, Messenger, Time Factors, Gene Expression, Rats, Wistar, Adipocytes, Peptide Elongation Factor 2, PPAR gamma, Adipogenesis, Fatty Acid-Binding Proteins, Rats, Adipose Tissue, White

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 ›

Are you an author, or do you see a problem with this page? Request a review