Pouriayevali Farnaz, Tavalaee Marziyeh, Taktaz-Hafshejani Taghi, Dattilio Maurizio, Nasr-Esfahani Mohammad H
Department of Clinical Sciences, Faculty of Veterinary Medicine, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran.
Department of Animal Biotechnology, Reproductive Biomedicine Research Center, Royan Institute for Biotechnology, Isfahan, Iran.
Andrologia. 2022 Dec;54(11):e14592. doi: 10.1111/and.14592. Epub 2022 Sep 19.
In this study, the effect of 14 weeks of standard diet (controls) or folate and vitamin B12-free diet (VBD group) or vitamin D-free diet (VDD group) were assessed on mice testicular function, and sperm function. Vitamin D deprivation caused increased body weight with no effect from VBD confirming the calcium-independent role of vitamin D on body weight homeostasis. The two deprivations caused convergent damages including decreased testosterone, worsened Johnson scores, tubular differentiation index and spermatogenesis index, and serious worsening of sperm parameters and of sperm functional tests (DNA methylation, protamination, DNA damage and lipid peroxidation). From a metabolic point of view, the damage from both models converged on the one carbon cycle (methylations) and the transsulfuration pathway (GSH and antioxidant defences) and increased circulating homocysteine, although with different mechanisms: VBD appeared to hamper methylations due to lower ability to regenerate homocysteine to methionine whereas VDD appeared to interfere with homocysteine transsulfuration to cysteine and, thereafter, GSH. VDD also caused a huge paradox increase of vitamin B12, which was likely in a non-functional form and warrants further investigation. These findings strongly endorse the potential benefit of combined folate/B12 and vitamin D supplementation in infertile patients.
在本研究中,评估了14周标准饮食(对照组)、无叶酸和维生素B12饮食(VBD组)或无维生素D饮食(VDD组)对小鼠睾丸功能和精子功能的影响。维生素D缺乏导致体重增加,VBD组则无此影响,这证实了维生素D在体重稳态方面的钙非依赖性作用。这两种缺乏导致了趋同的损害,包括睾酮降低、约翰逊评分恶化、生精小管分化指数和精子发生指数下降,以及精子参数和精子功能测试(DNA甲基化、鱼精蛋白、DNA损伤和脂质过氧化)严重恶化。从代谢角度来看,两种模型的损害都集中在一碳循环(甲基化)和转硫途径(谷胱甘肽和抗氧化防御)上,并导致循环同型半胱氨酸增加,尽管机制不同:VBD组似乎由于将同型半胱氨酸再生为甲硫氨酸的能力较低而阻碍甲基化,而VDD组似乎干扰同型半胱氨酸向半胱氨酸的转硫,进而影响谷胱甘肽。VDD组还导致维生素B12大幅反常增加,这可能是无功能形式,值得进一步研究。这些发现有力地支持了联合补充叶酸/B12和维生素D对不育患者的潜在益处。