Impaired hormonal responses to hypoglycemia in spontaneously diabetic and recurrently hypoglycemic rats. Reversibility and stimulus specificity of the deficits.

AM Powell, RS Sherwin… - The Journal of clinical …, 1993 - Am Soc Clin Investig
AM Powell, RS Sherwin, GI Shulman
The Journal of clinical investigation, 1993Am Soc Clin Investig
To evaluate the roles of iatrogenic hypoglycemia and diabetes per se in the pathogenesis of
defective hormonal counterregulation against hypoglycemia in insulin-dependent diabetes
mellitus (IDDM), nondiabetic, and spontaneously diabetic BB/Wor rats were studied using a
euglycemic/hypoglycemic clamp. In nondiabetic rats, recurrent (4 wk) insulin-induced
hypoglycemia (mean daily glucose, MDG, 59 mg/dl) dramatically reduced glucagon and
epinephrine responses by 84 and 94%, respectively, to a standardized glucose fall from 110 …
To evaluate the roles of iatrogenic hypoglycemia and diabetes per se in the pathogenesis of defective hormonal counterregulation against hypoglycemia in insulin-dependent diabetes mellitus (IDDM), nondiabetic, and spontaneously diabetic BB/Wor rats were studied using a euglycemic/hypoglycemic clamp. In nondiabetic rats, recurrent (4 wk) insulin-induced hypoglycemia (mean daily glucose, MDG, 59 mg/dl) dramatically reduced glucagon and epinephrine responses by 84 and 94%, respectively, to a standardized glucose fall from 110 to 50 mg/dl. These deficits persisted for > 4 d after restoring normoglycemia, and were specific for hypoglycemia, with normal glucagon and epinephrine responses to arginine and hypovolemia, respectively. After 4 wk of normoglycemia, hormonal counterregulation increased, with the epinephrine, but not the glucagon response reaching control values. In diabetic BB rats (MDG 245 mg/dl with intermittent hypoglycemia), glucagon and epinephrine counterregulation were reduced by 86 and 90%, respectively. Chronic iatrogenic hypoglycemia (MDG 52 mg/dl) further suppressed counterregulation. Prospective elimination of hypoglycemia (MDG 432 mg/dl) improved, but did not normalize hormonal counterregulation. In diabetic rats, the glucagon defect appeared to be specific for hypoglycemia, whereas deficient epinephrine secretion also occurred during hypovolemia. We concluded that both recurrent hypoglycemia and the diabetic state independently lead to defective hormonal counterregulation. These data suggest that in IDDM iatrogenic hypoglycemia magnifies preexisting counterregulatory defects, thereby increasing the risk of severe hypoglycemia.
The Journal of Clinical Investigation