کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2596825 | 1562398 | 2009 | 6 صفحه PDF | دانلود رایگان |
The present study was undertaken to investigate the hyperglycemic potential of acute exposure to acephate and its etiology employing rat model system. Oral administration of acephate (140 mg/kg b.w.) caused reversible hyperglycemia as evidenced by peak increase in blood glucose at 2 h after the administration (87% over control) followed by trend of normalization. In further experiment carried out to understand the etiology of the induced hyperglycemia, we observed that 2 h exposure to acephate caused significant increase in blood glucose, plasma corticosterone (78%) and activities of two gluconeogenesis enzymes in liver viz., glucose-6-phosphatase (91%) and tyrosine aminotransferase (84%) compared to that in control. When rats were exposed to acephate for 6 h, decrement was observed in elevated levels of blood glucose, plasma corticosterone and the gluconeogenesis enzymes of the liver. Adrenal cholesterol levels in acephate-exposed rats were significantly depleted. While the glycogen content in liver of 2-h exposure group was comparable to control, a tremendous increase in liver glycogen content (∼3.5 folds) was observed in rats of the 6-h exposure group. Our results demonstrate that acephate causes reversible hyperglycemia in rats probably by enhancing hepatic glucose output via gluconeogenesis. A role for hyperactivity of adrenal cortex is suggested in increased gluconeogenesis while significant attenuation in elevated levels of blood glucose and the activity the gluconeogenesis enzyme, glucose-6-phosphatase in liver with concomitant increase in liver glycogen are indicative of the onset of counter-regulatory responses such as hyperinsulinemia, to overcome the induced hyperglycemia.
Journal: Toxicology - Volume 257, Issues 1–2, 4 March 2009, Pages 40–45