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维生素 D 补充剂通过过氧化物酶体增殖物激活受体-γ/转化生长因子-β1/核因子-κB 改善糖尿病大鼠的睾丸功能。

Vitamin D supplementation improves testicular function in diabetic rats through peroxisome proliferator-activated receptor-γ/transforming growth factor-beta 1/nuclear factor-kappa B.

机构信息

Department of Endocrinology and Metabolism, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.

Institute of Clinical Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.

出版信息

J Diabetes Investig. 2019 Mar;10(2):261-271. doi: 10.1111/jdi.12886. Epub 2018 Aug 6.

DOI:10.1111/jdi.12886
PMID:29953732
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6400168/
Abstract

AIMS/INTRODUCTION: Vitamin D deficiency can lead to male hypogonadism in diabetes mellitus, but the target organs and the mechanism driving the disorder are unclear. This experiment was designed to study the relationship between vitamin D deficiency and hypogonadism in diabetes mellitus.

MATERIALS AND METHODS

Rats with streptozotocin-induced diabetes were randomly divided into four groups and treated with different doses of vitamin D : blank (no vitamin D ), low (0.025 μg/kg/day), high (0.1 μg/kg/day), high (0.1 μg/kg/day) and with bisphenol A diglycidyl ether (peroxisome proliferator-activated receptor gamma inhibitor 30 mg/kg/day). They were compared with wild-type rats.

RESULTS

After 12 weeks, the vitamin D supplements had partially restored testicular pathological changes, as shown by reduced testicular fibrosis related to downregulation transforming growth factor beta 1 and apoptosis related to downregulation of nuclear factor kappa B, but not the pituitary gland. The expression of peroxisome proliferator-activated receptor gamma, which can inhibit transforming growth factor beta 1 and nuclear factor kappa B, was significantly increased after treatment with vitamin D .

CONCLUSIONS

These results suggest that treatment with vitamin D can improve testicular function in diabetic rats through the peroxisome proliferator-activated receptor gamma/transforming growth factor beta 1/nuclear factor kappa B signaling pathway.

摘要

目的/引言:维生素 D 缺乏可导致糖尿病患者的男性性腺功能减退症,但靶器官和导致该疾病的机制尚不清楚。本实验旨在研究维生素 D 缺乏与糖尿病性腺功能减退症的关系。

材料和方法

链脲佐菌素诱导的糖尿病大鼠随机分为四组,分别用不同剂量的维生素 D 处理:空白(无维生素 D)、低(0.025μg/kg/天)、高(0.1μg/kg/天)和高(0.1μg/kg/天)加双酚 A 二缩水甘油醚(过氧化物酶体增殖物激活受体γ抑制剂 30mg/kg/天)。将它们与野生型大鼠进行比较。

结果

12 周后,维生素 D 补充部分恢复了睾丸的病理变化,表现为睾丸纤维化相关的转化生长因子β 1 下调和核因子 kappa B 相关的凋亡减少,但对垂体无影响。过氧化物酶体增殖物激活受体γ的表达显著增加,该受体可抑制转化生长因子β 1 和核因子 kappa B。

结论

这些结果表明,维生素 D 治疗可通过过氧化物酶体增殖物激活受体γ/转化生长因子β 1/核因子 kappa B 信号通路改善糖尿病大鼠的睾丸功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/ce1b10b98090/JDI-10-261-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/2f912beca1d1/JDI-10-261-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/42953939c40f/JDI-10-261-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/e5d7677e1701/JDI-10-261-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/be43713c9269/JDI-10-261-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/090fe0bdc5ac/JDI-10-261-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/da276059a1a6/JDI-10-261-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/ce1b10b98090/JDI-10-261-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/2f912beca1d1/JDI-10-261-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/42953939c40f/JDI-10-261-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/e5d7677e1701/JDI-10-261-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/be43713c9269/JDI-10-261-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/090fe0bdc5ac/JDI-10-261-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/da276059a1a6/JDI-10-261-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d121/6400168/ce1b10b98090/JDI-10-261-g007.jpg

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