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Published on: October 20, 2017
Vitamin D supplement improved testicular function in diabetic rats
Chenzhao Ding1, Qinzhu Wang2, Yue Hao1
1Division of Endocrinology, Department of Internal Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China; Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Abstract:
This study was designed to investigate the role that 1,25(OH)2D3 plays against testicular lesion in diabetic rats and try to find its possible mechanism of the steroidogenesis and the spermatogenesis. In diabetic rats, prolonged hyperglycemia evaluated inflammatory cytokines, damaged sperm production function and redox balance, diminished serum testosterone. After treated with 1,25(OH)2D3 at two different doses respectively for 12 months, all the alternations were effectively normalized. 1,25(OH)2D3 showed inhibitory effect on excessive inflammatory biomarkers and adjusted the expression reproductive genes and testicular androgen synthesis. It also upregulated Bcl-2 expression, decreased Bax and COX-2 expression and inhibited active caspase cascade (caspase 8 and caspase 3), which may preserved the testicular cells under diabetic condition. It revealed that vitamin D supplement may protect the cells through suppressing inflammation factors and alleviating cell apoptotic death, as well as upregulating the expression of genes related to reproductive and testosterone synthesis.
Insights
Vitamin D (1,25(OH)2D3) supplementation effectively reversed testicular damage in diabetic rats. This vitamin D treatment normalized testosterone levels, improved sperm production, and reduced inflammation and cell death.
Area of Science:
- Endocrinology
- Reproductive Biology
- Diabetology
Background:
- Diabetes mellitus causes testicular dysfunction, characterized by inflammation, impaired sperm production, and reduced testosterone.
- Hyperglycemia in diabetes negatively impacts redox balance and elevates inflammatory cytokines, contributing to testicular damage.
Purpose of the Study:
- To investigate the protective effects of 1,25(OH)2D3 against testicular lesions in a diabetic rat model.
- To elucidate the mechanisms underlying 1,25(OH)2D3's influence on steroidogenesis and spermatogenesis in diabetic conditions.
Main Methods:
- Diabetic rats were treated with two different doses of 1,25(OH)2D3 for 12 months.
- Assessment of inflammatory biomarkers, sperm production, redox balance, serum testosterone, gene expression (reproductive genes, Bcl-2, Bax, COX-2), and caspase activity.
Main Results:
- 1,25(OH)2D3 treatment normalized hyperglycemia-induced alterations, including inflammation and impaired sperm function.
- The vitamin D compound effectively adjusted reproductive gene expression and testicular androgen synthesis.
- Upregulation of Bcl-2 and downregulation of Bax and COX-2 were observed, alongside inhibition of caspase cascade, indicating reduced apoptosis.
Conclusions:
- Vitamin D supplementation demonstrates a protective role against testicular damage in diabetic rats.
- 1,25(OH)2D3 mitigates testicular injury by suppressing inflammation, alleviating apoptotic cell death, and enhancing reproductive and testosterone synthesis pathways.
