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Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats

OBJECTIVE: In diabetes mellitus, vitamin D(3) deficiency affects sex hormone levels and male fertility; however, the mechanism leading to the disorder is unclear. This research was designed to investigate the mechanism of vitamin D(3) deficiency and hypogonadism in diabetic rats. Our aim was to asse...

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Autores principales: He, Yanyan, Liu, Yang, Wang, Qing-Zhu, Guo, Feng, Huang, Fengjuan, Ji, Linlin, An, Tingting, Qin, Guijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589201/
https://www.ncbi.nlm.nih.gov/pubmed/31281852
http://dx.doi.org/10.1155/2019/7894950
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author He, Yanyan
Liu, Yang
Wang, Qing-Zhu
Guo, Feng
Huang, Fengjuan
Ji, Linlin
An, Tingting
Qin, Guijun
author_facet He, Yanyan
Liu, Yang
Wang, Qing-Zhu
Guo, Feng
Huang, Fengjuan
Ji, Linlin
An, Tingting
Qin, Guijun
author_sort He, Yanyan
collection PubMed
description OBJECTIVE: In diabetes mellitus, vitamin D(3) deficiency affects sex hormone levels and male fertility; however, the mechanism leading to the disorder is unclear. This research was designed to investigate the mechanism of vitamin D(3) deficiency and hypogonadism in diabetic rats. Our aim was to assess serum vitamin D(3) levels and the relationship among vitamin D(3), insulin-like growth factor-1 (IGF-1), and testicular function. MATERIALS AND METHODS: Rats with streptozotocin-induced diabetes were randomly divided into four groups and treated with different doses of vitamin D(3): no vitamin D(3), low (0.025 μg/kg/day), high (0.1 μg/kg/day), and high (0.1 μg/kg/day) with JB-1 (the insulin-like growth factor-1 receptor inhibitor group, 100 μg/kg/day). The groups were compared with wild-type rats, which function as the control group. Various parameters such as vitamin D(3) and IGF-1 were compared between the experimental and wild-type groups, and their correlations were determined. RESULTS: Twelve weeks of vitamin D(3) supplementation improved the testosterone levels, as shown by the increase in the level of serum IGF-1 in diabetic rats. Phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT), which was a downstream of the signaling pathway of IGF-1, was significantly increased after vitamin D(3) treatment. CONCLUSIONS: The study shows that vitamin D(3) may promote the expression of testosterone and improve testicular function in diabetic rats by activating PI3K/AKT via IGF-1.
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spelling pubmed-65892012019-07-07 Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats He, Yanyan Liu, Yang Wang, Qing-Zhu Guo, Feng Huang, Fengjuan Ji, Linlin An, Tingting Qin, Guijun J Diabetes Res Research Article OBJECTIVE: In diabetes mellitus, vitamin D(3) deficiency affects sex hormone levels and male fertility; however, the mechanism leading to the disorder is unclear. This research was designed to investigate the mechanism of vitamin D(3) deficiency and hypogonadism in diabetic rats. Our aim was to assess serum vitamin D(3) levels and the relationship among vitamin D(3), insulin-like growth factor-1 (IGF-1), and testicular function. MATERIALS AND METHODS: Rats with streptozotocin-induced diabetes were randomly divided into four groups and treated with different doses of vitamin D(3): no vitamin D(3), low (0.025 μg/kg/day), high (0.1 μg/kg/day), and high (0.1 μg/kg/day) with JB-1 (the insulin-like growth factor-1 receptor inhibitor group, 100 μg/kg/day). The groups were compared with wild-type rats, which function as the control group. Various parameters such as vitamin D(3) and IGF-1 were compared between the experimental and wild-type groups, and their correlations were determined. RESULTS: Twelve weeks of vitamin D(3) supplementation improved the testosterone levels, as shown by the increase in the level of serum IGF-1 in diabetic rats. Phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT), which was a downstream of the signaling pathway of IGF-1, was significantly increased after vitamin D(3) treatment. CONCLUSIONS: The study shows that vitamin D(3) may promote the expression of testosterone and improve testicular function in diabetic rats by activating PI3K/AKT via IGF-1. Hindawi 2019-06-04 /pmc/articles/PMC6589201/ /pubmed/31281852 http://dx.doi.org/10.1155/2019/7894950 Text en Copyright © 2019 Yanyan He et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
He, Yanyan
Liu, Yang
Wang, Qing-Zhu
Guo, Feng
Huang, Fengjuan
Ji, Linlin
An, Tingting
Qin, Guijun
Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats
title Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats
title_full Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats
title_fullStr Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats
title_full_unstemmed Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats
title_short Vitamin D(3) Activates Phosphatidylinositol-3-Kinase/Protein Kinase B via Insulin-Like Growth Factor-1 to Improve Testicular Function in Diabetic Rats
title_sort vitamin d(3) activates phosphatidylinositol-3-kinase/protein kinase b via insulin-like growth factor-1 to improve testicular function in diabetic rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6589201/
https://www.ncbi.nlm.nih.gov/pubmed/31281852
http://dx.doi.org/10.1155/2019/7894950
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