Abstract
Glucose is a major physiological stimulator of insulin secretion in the islets of the pancreas. However, the islets of fetal and perinatal animals have been shown to be poorly responsive to glucose stimulation in insulin release compared to adult islets. The present investigation was thus undertaken to determine whether the adrenergic mechanism participated in the poor insulin responsiveness of neonatal islets.
Islets isolated by the collagenase method from rats of the 1st, 3rd and 7th day after birth and from adult rats were incubated in a standard medium of Krebs-Henseleit bicarbonate buffer containing various concentrations of glucose, epinephrine and/or phentolamine for 60 min subsequent to a 20-min preincubation at 37°C under a gas phase of 95% O2: 5% CO2. The insulin released into the medium was estimated by radioimmunoassay.
The insulin responsiveness to glucose of the islets from rats of the 1st day after birth was lower than that of adult rats. However, the responsiveness of rats on the 3rd and 7th post-natal days was similar to that of adult rats. The suppressive effect of epinephrine on insulin release from the islets of the 1st post-natal day was poor compared to that the that of adult rats. Phentolamine at a concentration of 0.01 to 0.1 mM increased the insulin responsiveness to glucose, but the enhancement declined with age. At 1 mM, phentolamine suppressed the insulin responsiveness in adult rats, but it was increased in neonates.
These observations suggest that the endogenous a-adrenergic mechanism may be functioning during the neonatal periods and be involved in the poor insulin responsiveness of rats immediately after birth.
