Fetal (20–21 day gestation) and neonatal (<5-day-old) rat islets were isolated from the glucagon-rich (dorsal) and glucagon-poor (ventral) pancreatic regions. After 1 or 2 wk in culture, groups of islets from each region were transferred to culture dishes containing Krebs-Ringer bicarbonate buffer with low (2.4 mM) and high (16.7 mM) glucose plus aminophylline. After 2 wk in culture, insulin released into medium was higher than after 1 wk, and more so if the islets originated from dorsal tissue (P < .01). Glucagon release in response to alanine (10 mM) stimulation was also significantly higher in dorsal than in ventral islets (6.38 ± 1.98 vs. 1.49 ± 0.89 pg · islet−1 · h−1 respectively; P < .02).

Coincident with higher insulin and glucagon release, islet yield was greater in tissue from the dorsal neonatal pancreas than from that obtained in the fetal and neonatal ventral pancreas [range: dorsal, 131–180 (median, 153), vs. ventral, 53–127 (median, 84), islets obtained on day 5 of culture].

Neonatal islets of dorsal origin were transplanted intrasplenically (500–3000 islets) to streptozocin-induced diabetic inbred Lewis rats. Only rats receiving >2500 islets were cured by transplantation.

These experiments show that dorsal fetal islets secrete more insulin than do ventral islets and that islet yield is higher when islets are isolated from dorsal rather than from ventral perinatal pancreatic tissue. Despite their in vitro behavior, more neonatal dorsal islets are required to cure experimental diabetes than are reported With adult islets.

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