Insulin release after acute hydrocortisone treatment in mice.
This investigation examined a potential mechanism for the inhibition of insulin release following an acute dose of hydrocortisone sodium succinate (HC). Hydrocortisone (300 mg/kg intraperitoneally) elevated plasma glucose levels (P less than or equal to 0.05) when administered to male Swiss-Webster mice, without altering plasma insulin levels. This results in a significantly lower insulinogenic index (P less than or equal to 0.05). Hydrocortisone suppressed the glucose-stimulated insulin levels (P less than or equal to 0.05) following an intravenous glucose challenge (2 g/kg) in both fed and fasted mice. Pretreatment with chlorisondamine (EC) and phentolamine (PT) did not alter the HC-induced hyperglycemia but did result in higher plasma insulin levels in response to the higher glucose levels. Adrenalectomy did not prevent the HC-depressed insulin response to hyperglycemia. This is consistent with the hypothesis that an acute dose of HC may be indirectly suppress insulin release by central activation of the sympathetic nerves at the pancreatic islets.
D000315:Adrenalectomy; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002714:Chlorisondamine / Q000494:pharmacology; D005951:Glucose Tolerance Test; D006854:Hydrocortisone / Q000494:pharmacology*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D051379:Mice; D010646:Phentolamine / Q000494:pharmacology
D001786:Blood Glucose; D007328:Insulin; D002714:Chlorisondamine; D006854:Hydrocortisone; D010646:Phentolamine