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Effect of Vitamin D3 on Uterine Morphology and Insulin Signaling in a Polycystic Ovary Syndrome (PCOS) Rat Model

Open Access
|Oct 2024

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrinopathy in women of reproductive age leading to infertility. Besides reproductive and hormonal disturbances, PCOS is often characterized by vitamin D3 (VD) deficiency. This study aimed to determine the effect of VD on uterine histoarchitecture, the biochemical composition of gland secretions, and the insulin signal transduction pathway using a PCOS rat model. The experiment was conducted on four animal groups (n=8/group): control (C), VD supplemented (VD; 500 IU/day), letrozole-treated (PCOS; 1 mg/kg body weight), and VD-treated PCOS (PCOS+VD) group. Herein, VD supplementation did not improve histomorphometric parameters in the PCOS uterus, whereas clearly influenced sugar composition in uterine gland secretions, restoring their content to that observed in the C group. Furthermore, we found that VD can reduce peripheral and local uterine insulin resistance developed in the PCOS rats via activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway and subsequent glucose metabolism in the uterus. To sum up, the present results suggest a possible beneficial role of VD supplementation for the maintenance of uterus functions in PCOS rats.

DOI: https://doi.org/10.2478/aoas-2024-0038 | Journal eISSN: 2300-8733 | Journal ISSN: 1642-3402
Language: English
Page range: 1197 - 1209
Submitted on: Sep 19, 2023
Accepted on: Feb 21, 2024
Published on: Oct 24, 2024
Published by: National Research Institute of Animal Production
In partnership with: Paradigm Publishing Services
Publication frequency: 4 times per year

© 2024 Kinga Kamińska, Marcelina Tchurzyk, Olga Fraczek, Agata Szlaga, Patryk Sambak, Szymon Tott, Kamilla Małek, Katarzyna Knapczyk-Stwora, Anna Błasiak, Agnieszka Rak, Małgorzata Grzesiak, published by National Research Institute of Animal Production
This work is licensed under the Creative Commons Attribution 4.0 License.