In developmental terms, the endocrine system of neither the gut nor the pan
creatic islets has been characterized fully. Little is known about the invo
lvement of cholecystokinin (CCK), a gut hormone, involved in regulating the
secretion of pancreatic hormones, and pancreatic growth. Here. we tracked
CCK-expressing cells in the intestines and pancreata of normal mice (BALB/c
), Non Obese Diabetic (NOD) mice and interferon (IFN)-gamma transgenic mice
, which exhibit pancreatic regeneration, during embryonic development, the
postnatal period and adulthood. We also questioned whether IFN-gamma influe
nces the expression of CCK. The results from embryonic day 16 showed that a
ll three strains had CCK in the acinar region of pancreata, and specificall
y in alpha cells that also expressed glucagon. However, in adulthood only B
ALB/c and NOD mice continued this pattern. By contrast, in IFN-gamma transg
enic mice, CCK expression was suppressed from birth to 3 months of age in t
he pancreata but not intestines. However, by 5 months of age, CCK expressio
n appeared in the regenerating pancreatic ductal region of IFN-gamma transg
enic mice. In the intestine, CCK expression persisted from fetus to adultho
od and was not influenced by IFN-gamma. Intestinal cells expressing CCK did
not co-express glucagon, suggesting that these cells are phenotypically di
stinct from CCK-expressing cells in the pancreatic islets, and the effect o
f IFN-gamma on CCK varies depending upon the cytokine's specific microenvir
onment.