We investigated the effects of methimazole, an anti-thyroid drug, on the onset of type 2 diabetes in Zucker diabetic fatty (ZDF) rats. For this, 0.03% methimazole was administered to 7-week-old, pre-diabetic ZDF rats in drinking water for 5 weeks and the animals were sacrificed at 12 weeks of age. Methimazole treatment to ZDF rats significantly reduced blood glucose levels, food intake, body weight, and serum T3 levels. Hepatocytes in ZDF-methi rats were more densely stained with eosin than those in ZDF rats because of low fat accumulation in ZDF-methi hepatocytes. The pancreatic islet in ZDF-methi rats was normal compared to that in ZDF rats. Glucagon, not insulin, immunoreactivity in ZDF-methi rats was significantly higher than that in ZDF-methi rats. These suggest that methimazole treatment may delay the onset of type 2 diabetes in leptin receptor-deficient rats and also suggests that thyroid hormones may be necessary for the onset of diabetes.

To explore the effects of radiofrequency electromagnetic field on the fate of neuronal cells, we investigated whether exposure to 915 MHz radiofrequency identification (RFID) caused morphological changes in neuronal cells in rat hippocampal dentate gyrus (DG). A reverberation chamber was used as a whole-body RFID exposure system. Rats were assigned to two groups: sham-and RFID-exposed groups. Rats in the RFID-exposed group were exposed to RFID at 4 W/kg specific absorption rate (SAR) for 8 hours daily, 5 days per week, for 2 weeks. Morphological evaluation of DG was performed using immunohistochemistry with doublecortin (DCX) as a neuronal precursor cell marker and neuronal nuclei (NeuN) as a mature neuronal cell marker. No significant morphological changes in DCX+ or NeuN+ cells in the DG of RFID-exposed rats were observed. These results suggest that RFID exposure induces no significant change in DCX+ neuronal precursor or NeuN+ neuronal cells in DG of rats.