Glucose Affectsin VitroMaturation of Fetal Rat Islets*

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Abstract
Fetal pancreatic islets (21.5 day old) were cultured in RPMI 1640 containing either 2.8 or 11.1 mM glucose for 7 days. After the 7-day culture period, islets cultured in 2.8 mM glucose demonstrated a minimal first phase of insulin secretion in response to acute glucose stimulation, while islets cultured in 11.1 mM glucose demonstrated a biphasic insulin secretory pattern. Islets cultured in 11.1 mM glucose initiated insulin secretion at 4.4 .+-. 0.1 mM glucose and plateaued at 11.6 mM glucose when exposed to a linear gradient. In addition, culture in 11.1 mM glucose increased DNA content (P < 0.01) and [3H]thymidine incorporation (P < 0.05) in fetal islets. The actual number of .beta.-cells within islets cultured in either 2.8 or 11.1 mM glucose did not increase. The insulin contents of islets cultured in 2.8 and 11.1 mM glucose were 0.46 .+-. 0.06 and 1.14 .+-. 0.10 mU/islet, respectively. During subsequent glucose stimulation, islets cultured in 2.8 and 11.1 mM glucose released 3% and 5.6% of their total insulin content, respectively. Ultrastructural morphometric analysis indicated that 11.1 mM glucose stimulated an increase in the volume of individual .beta.-cells, i.e., hypertrophy. The hypertrophy of .beta.-cells within islets cultured in 11.1 mM glucose resulted in a concomitant increases in islet volume. Finally, the hypertrophy of .beta.-cells within islets cultured in 11.1 mM glucose was a result of increased volumes of mitochondria, secretory granules, and, to the greatest extent, endoplasmic reticulum. Glucose is a potent factor in the maturation of cultured fetal rat islets.