Diabetes mellitus (DM) is associated with increased risk of reproductive problems. Estrogens have important roles in reproductive processes in both genders. Aromatase catalyzes the conversion of androgens to estrogens and is expressed in a variety of tissues. Although it is known that insulin regulate the activity of aromatase, there are few data about the effects of diabetes on this enzyme. The aim of the present study was to investigate the effects of experimental diabetes on aromatase expression levels in ovary, testis, uterus, and vas deferens tissues of female and male rats. Rats were injected with streptozotocin to induce diabetes. At the end of 4 and 12 weeks, tissue homogenates were prepared and evaluated for aromatase proteins by western blot. Uterus and vas deferens smooth muscle responses were also evaluated. Aromatase expression levels in ovary were significantly decreased both in 4 and 12 weeks of diabetes. In testis, enzyme levels were not altered at 4 weeks, but significantly decreased at 12 weeks of diabetes. In uterus and vas deferens tissues, no significant differences were observed at aromatase immunoreactivity but uterus and vas deferens smooth muscle responses were altered. These results indicated for the first time that DM altered the expression levels of aromatase both in ovary and testis but did not affect enzyme levels in uterus and vas deferens tissues. Altered smooth muscle responses did not correlate with tissue aromatase levels. Altogether, these findings lead us to suggest that aromatase might be an important target molecule in sexual dysfunction seen in DM.

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Our data suggest that insulin deprivation, rather than high glucose, is a significant determinant of IDE regulation. As evidence indicates potential roles for IDE in diabetes and AD, understanding the mechanisms regulating IDE expression may be important in developing new treatment strategies.

Diabetes mellitus (DM) is associated with increased risk of impaired cognitive function. Diabetic neuropathy is one of the most common and important complications of DM. Estrogens prevent neuronal loss in experimental models of neurodegeneration and accelerate nerve regeneration. Aromatase catalyzes the conversion of androgens to estrogens and expressed in a variety of tissues including neurons. Although insulin is known to regulate the activity of aromatase there is no study about the effects of diabetes on this enzyme. Present study was designed to investigate the effects of experimental diabetes on aromatase expression in nervous system. Gender-based differences were also investigated. Rats were injected with streptozotocin to induce diabetes. At the end of 4 and 12 weeks sciatic nerve and hippocampus homogenates were prepared and evaluated for aromatase proteins. Aromatase expressions in sciatic nerves of both genders were decreased in 4 weeks of diabetes, but in 12 weeks the enzyme levels were increased in females and reached to control levels in male animals. Aromatase levels were not altered in hippocampus at 4 weeks but increased at 12 weeks in female diabetic rats. No significant differences were observed at enzyme levels of hippocampus in male diabetic rats. Insulin therapy prevented all diabetes-induced changes. In conclusion, these results indicated for the first time that, DM altered the expression of aromatase both in central and peripheral nervous systems. Peripheral nervous system is more vulnerable to damage than central nervous system in diabetes. These effects of diabetes differ with gender and compensatory neuroprotective mechanisms are more efficient in female rats.