Evidence suggests that oestrogen has both protective and damaging effects in the body. Circulating oestrogens are transported in the blood as inactive forms, as they are bound to sulphates. These sulphate groups must be removed to activate these oestrogens and this is done by the enzyme steroid sulphatase. Thus, expression and activity of steroid sulphatase is directly related to the formation of active oestrogens, and therefore impacts oestrogen-related pathologies.
A recent study published in the Journal of Biology and Chemistry, now suggests that steroid sulphatase, when over-expressed in the liver, can protect against obesity and type-2 diabetes in mice. In females, this effect is directly related to increased active oestrogens levels. Interestingly, steroid sulphatase expression and activity were increased in mice fed a high-fat diet, and when they were fasting. This suggests that steroid sulphatase may respond during stress, suggesting this enzyme link with potential protective mechanisms within the liver.
Our own recent data suggests that, in colorectal cancer, steroid sulphatase activity is up-regulated during inflammation. We speculate that this may be an attempted protective response, as elevated active oestrogen concentrations are known to induce apoptosis in non-malignant colorectal cells.
Thus, our work currently supports the concept outlines in the Journal of Biology and Chemistry paper that steroid sulphatase may be a stress-response enzyme that actively drives local active oestrogen concentrations, and therefore regulates cell survival.
Further work should now been done to examine whether inhibition of steroid sulphatase activity has detrimental effects on type-2 diabetes, obesity, and other forms of metabolic syndrome.