Does Vitamin A play A Role In Testosterone Regulation?

There is an enzyme in the body that is responsible for converting beta carotene from the dietary carotenoid into vitamin A – the functional form that is used by the body. According to a recent study, the very same enzyme also plays a key role in the regulation of the testosterone levels and acts as a precursor of prostate growth. The enzyme is called Bco1 and it was studied at the University of Illinois as it effects the testosterone levels and tissues with testosterone sensitivity like prostate. The comparative study was based on the laboratory mice with missing functional Bco1 gene and mice of the control group.

Inside the human body, this enzyme breaks the single beta-carotene molecule (which gives orange coloration to pumpkin, carrots and various other plants) to yield two vitamin A molecules. Scientists have proposed that Bco1 may also regulate some other biological processes.

Relationship Between Bco1 Gene Variations And Testosterone Levels

Studies conducted in the past have revealed that mice with no Bco1 gene fails to split the beta carotene molecules and due to variation in Bco1 gene, it is likely to have the carotenoid metabolism affected up to certain extent. Therefore Joshua W. Smith, paper’s lead author suggested, there are chances that men having Bco1 gene variation may as well experience alteration in the levels of testosterone.

The two mice groups were given a beta-carotene and carotenoid free diet but provided them with sufficient amount of vitamin A to normalize the liver and blood nutrients. The mice group that lacked Bco1 gene showed low levels of testosterone and the size of prostate was comparably small.

As testosterone is essential in developing and maintaining seminal vesicles and prostates, so in Bco1 lacking group, the weight of seminal vesicles and prostate was 20-30% less in contrast to the controlled group. The Bco1 lacking group also showed 44% lower concentration of leydig cells (cells responsible for the conversion of cholesterol into testosterone).

The Bco1 lacking group also exhibited 32% reduction in Hsd17b3 gene levels (involved in the synthesis of testosterone from leydig cells).

In men, hereditary alterations/variations in Hsd17b3 gene can lead to:

• Evident deficiency of testosterone production
• Feminized genitalia at the time of birth

The scientists examined 200 genes present in the prostate of tested mice out of which 13 were found to be altered by the absence of Bco1. 3 of these altered genes were noted to be involved in the proliferation of cell, one involved in the epithelial tissues and stromal growth, two involved in the cell cycle progression whereas one involved in apoptosis; cell death.

The researchers also discovered that the Bco1 lacking group exhibited disrupted signaling of androgen receptors which is very essential for development and functioning of prostate and regulation of gene expression. According to the study, the AR signaling also plays a role in the initiation and progression of prostate cancer.

The findings of the study elaborated on how Bco1 is capable of performing other physiological functions along with its primary function of cleaving carotenoid and how the lacking of this enzyme can adversely affect:

• The AR signaling
• Androgen synthesis
• Cellular proliferation
• Prostate growth

References

• Smith, J. W., Ford, N. A., Thomas-Ahner, J. M., Moran, N. E., Bolton, E. C., Wallig, M. A., ... & Erdman, J. W. (2016). Mice lacking β-carotene-15, 15’-dioxygenase exhibit reduced serum testosterone, prostatic androgen receptor signaling, and prostatic cellular proliferation. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 311(6), R1135-R1148.