Diabetes alters aromatase enzyme levels in sciatic nerve and hippocampus tissues of rats.
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.
Burul-Bozkurt
Nihan
N
Faculty of Pharmacy, Department of Pharmacology, Hacettepe University, Sihhiye, Ankara, Turkey. nihanb@hacettepe.edu.tr
Pekiner
Can
C
Kelicen
Pelin
P
D000818:Animals; D001141:Aromatase / Q000032:analysis / Q000378:metabolism*; D001928:Brain Diseases, Metabolic / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology; D003072:Cognition Disorders / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology; D019610:Cytoprotection / Q000502:physiology*; D048909:Diabetes Complications / Q000201:enzymology* / Q000503:physiopathology; D003921:Diabetes Mellitus, Experimental; D003929:Diabetic Neuropathies / Q000201:enzymology / Q000503:physiopathology; D004195:Disease Models, Animal; D004967:Estrogens / Q000096:biosynthesis*; D005260:Female; D006624:Hippocampus / Q000201:enzymology / Q000503:physiopathology; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009410:Nerve Degeneration / Q000201:enzymology / Q000209:etiology / Q000503:physiopathology; D009416:Nerve Regeneration / Q000502:physiology; D018696:Neuroprotective Agents / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000201:enzymology / Q000503:physiopathology; D012727:Sex Characteristics
D004967:Estrogens; D007328:Insulin; D018696:Neuroprotective Agents; D001141:Aromatase