An enzyme that converts the dietary carotenoid beta carotene into vitamin A in the body may also regulate testosterone levels and growth of the prostate, a new study found. Scientists at the University of Illinois explored the impact of the enzyme Bco1 on testosterone levels and testosterone-sensitive tissues such as the prostate by comparing the prostatic function and testosterone metabolism of mice that lacked functional copies of the Bco1 gene with mice in the control group.
Both groups of mice were fed a diet free of beta carotene and other carotenoids but which provided vitamin A to maintain normal levels of that nutrient in their blood and livers.
As the researchers hypothesized, mice lacking Bco1 had lower blood concentrations of testosterone. In examining the rodents’ tissues, the researchers found that the prostates were significantly smaller in mice without the Bco1 gene.
These animals’ prostates and seminal vesicles – both of which require testosterone for normal development and maintenance – weighed 20 to 30 percent less than those of the other mice. The Bco1-null mice also had 44 percent fewer Leydig cells in their testes – the cells that convert cholesterol into testosterone.
Additionally, the mice without the Bco1 gene had 32 percent lower levels of the Hsd17b3 gene, which is expressed exclusively in the Leydig cells of the testes and is responsible for the final step of testosterone synthesis.
Original press release.
Both groups of mice were fed a diet free of beta carotene and other carotenoids but which provided vitamin A to maintain normal levels of that nutrient in their blood and livers.
As the researchers hypothesized, mice lacking Bco1 had lower blood concentrations of testosterone. In examining the rodents’ tissues, the researchers found that the prostates were significantly smaller in mice without the Bco1 gene.
These animals’ prostates and seminal vesicles – both of which require testosterone for normal development and maintenance – weighed 20 to 30 percent less than those of the other mice. The Bco1-null mice also had 44 percent fewer Leydig cells in their testes – the cells that convert cholesterol into testosterone.
Additionally, the mice without the Bco1 gene had 32 percent lower levels of the Hsd17b3 gene, which is expressed exclusively in the Leydig cells of the testes and is responsible for the final step of testosterone synthesis.
Original press release.
