Meiying Feng1, Kai Wang2, Hengxi Wei2, Shouquan Zhang2, Yun Chen3. 1. College of Life Sciences, Zhaoqing University, Zhaoqing, China. 2. Guangdong Provincial Key Laboratory of Agro-animal Genomics and Molecular Breeding, College of Animal Science, South China Agricultural University, Guangzhou, China. 3. Henry Fok College of Biology and Agriculture, Shaoguan University, Shaoguan, China.
Abstract
INTRODUCTION: The concentration of 25-hydroxycholecalciferol (25OHD3) in the serum of obese people is low and often accompanied by symptoms of low fertility. Therefore, vitamin D is recommended as a potential treatment option. However, after clinical trials, it was found that vitamin D cannot effectively increase the concentration of 25OHD3 in the serum of obese people. How obesity causes low 25OHD3 concentration and low fertility is unclear. METHODS: We analyzed the physiological and pathological changes in obese mice induced by a high-fat diet (HFD) and the changes in mice after supplementing with 25OHD3. RESULTS: The concentration of 25OHD3 in the serum of obese mice induced by HFD was significantly reduced, and these mice showed liver hypertrophy accompanied by abnormal liver injury, testicular hypertrophy, low testosterone levels, high leptin levels, and low sperm motility. The mRNA and protein expression of CYP2R1 of hydroxylated vitamin D3 was significantly reduced; CYP11A1 and CYP11A2, which synthesize testosterone, were significantly reduced. After supplementing with 25OHD3, there was an increase in serum 25OHD3 concentration, testosterone level, and sperm motility, but it cannot improve the degree of obesity, CYP2R1 expression, and liver damage. CONCLUSION: Our research shows that there is a metabolic interference mediated by 25OHD3 and testosterone between obesity and low sperm motility. The results of this study can provide a scientific basis for studying the mechanism of 25OHD3 and hormone regulation and treating obese people with low sperm motility.
INTRODUCTION: The concentration of 25-hydroxycholecalciferol (25OHD3) in the serum of obese people is low and often accompanied by symptoms of low fertility. Therefore, vitamin D is recommended as a potential treatment option. However, after clinical trials, it was found that vitamin D cannot effectively increase the concentration of 25OHD3 in the serum of obese people. How obesity causes low 25OHD3 concentration and low fertility is unclear. METHODS: We analyzed the physiological and pathological changes in obese mice induced by a high-fat diet (HFD) and the changes in mice after supplementing with 25OHD3. RESULTS: The concentration of 25OHD3 in the serum of obese mice induced by HFD was significantly reduced, and these mice showed liver hypertrophy accompanied by abnormal liver injury, testicular hypertrophy, low testosterone levels, high leptin levels, and low sperm motility. The mRNA and protein expression of CYP2R1 of hydroxylated vitamin D3 was significantly reduced; CYP11A1 and CYP11A2, which synthesize testosterone, were significantly reduced. After supplementing with 25OHD3, there was an increase in serum 25OHD3 concentration, testosterone level, and sperm motility, but it cannot improve the degree of obesity, CYP2R1 expression, and liver damage. CONCLUSION: Our research shows that there is a metabolic interference mediated by 25OHD3 and testosterone between obesity and low sperm motility. The results of this study can provide a scientific basis for studying the mechanism of 25OHD3 and hormone regulation and treating obese people with low sperm motility.
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