Vitamin D deficiency promotes prostatic hyperplasia in middle-age mice through exacerbating local inflammation

Vitamin D deficiency is especially prevalent in pregnant women and children. Our recent study demonstrated that vitamin D deficiency in early life disturbed testicular development. This study investigated the effects of vitamin D deficiency in early life on prostatic hyperplasia in middle-aged mice. In control group, dams and their male pups were fed with standard-chow diets. In VDD group, dams were fed with vitamin D deficient (VDD) diets throughout pregnancy and lactation. After weaning, male pups continued to be fed with VDD diets. As expected, prostate weight was elevated and prostatic hyperplasia was observed in VDD-fed mice. The number of prostatic Ki-67-positive epithelial cells, a proliferation marker, was increased in VDD-fed mice. Further analysis found that vitamin D deficiency promoted inflammatory infiltration and stromal fibrosis in prostate of middle-aged mice. Moreover, vitamin D deficiency activated NF-κB and up-regulated Il-6 mRNA in prostate of middle-aged mice. In addition, vitamin D deficiency activated prostatic STAT3, a proliferation pathway in middle-aged mice. Of interest, VDD-induced prostatic inflammation and hyperplasia were partially reversed when VDD diets was replaced with standard diets. These results provide evidence that vitamin D deficiency in early life promotes prostatic hyperplasia in middle-aged mice through exacerbating local inflammation.