Cholecystokinin expression in the developing and regenerating pancreas and intestine

G. Liu, S. V. Pakala, D. Gu, T. Krahl, L. Mocnik, N. Sarvetnick

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

In developmental terms, the endocrine system of neither the gut nor the pancreatic islets has been characterized fully. Little is known about the involvement 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)-γ transgenic mice, which exhibit pancreatic regeneration, during embryonic development, the postnatal period and adulthood. We also questioned whether IFN-γ influences the expression of CCK. The results from embryonic day 16 showed that all three strains had CCK in the acinar region of pancreata, and specifically in α cells that also expressed glucagon. However, in adulthood only BALB/c and NOD mice continued this pattern. By contrast, in IFN-γ transgenic mice, CCK expression was suppressed from birth to 3 months of age in the pancreata but not intestines. However, by 5 months of age, CCK expression appeared in the regenerating pancreatic ductal region of IFN-γ transgenic mice. In the intestine, CCK expression persisted from fetus to adulthood and was not influenced by IFN-γ. Intestinal cells expressing CCK did not co-express glucagon, suggesting that these cells are phenotypically distinct from CCK-expressing cells in the pancreatic islets, and the effect of IFN-γ on CCK varies depending upon the cytokine's specific microenvironment.

Original languageEnglish (US)
Pages (from-to)233-240
Number of pages8
JournalJournal of Endocrinology
Volume169
Issue number2
DOIs
StatePublished - May 28 2001

Fingerprint

Cholecystokinin
Intestines
Pancreas
Interferons
Transgenic Mice
Inbred NOD Mouse
Glucagon
Islets of Langerhans
Pancreatic Hormones
Endocrine System
Embryonic Development
Regeneration
Fetus
Parturition
Hormones
Cytokines

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Cholecystokinin expression in the developing and regenerating pancreas and intestine. / Liu, G.; Pakala, S. V.; Gu, D.; Krahl, T.; Mocnik, L.; Sarvetnick, N.

In: Journal of Endocrinology, Vol. 169, No. 2, 28.05.2001, p. 233-240.

Research output: Contribution to journalArticle

Liu, G. ; Pakala, S. V. ; Gu, D. ; Krahl, T. ; Mocnik, L. ; Sarvetnick, N. / Cholecystokinin expression in the developing and regenerating pancreas and intestine. In: Journal of Endocrinology. 2001 ; Vol. 169, No. 2. pp. 233-240.
@article{8ec310135ef24ce491951b30070e9258,
title = "Cholecystokinin expression in the developing and regenerating pancreas and intestine",
abstract = "In developmental terms, the endocrine system of neither the gut nor the pancreatic islets has been characterized fully. Little is known about the involvement 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)-γ transgenic mice, which exhibit pancreatic regeneration, during embryonic development, the postnatal period and adulthood. We also questioned whether IFN-γ influences the expression of CCK. The results from embryonic day 16 showed that all three strains had CCK in the acinar region of pancreata, and specifically in α cells that also expressed glucagon. However, in adulthood only BALB/c and NOD mice continued this pattern. By contrast, in IFN-γ transgenic mice, CCK expression was suppressed from birth to 3 months of age in the pancreata but not intestines. However, by 5 months of age, CCK expression appeared in the regenerating pancreatic ductal region of IFN-γ transgenic mice. In the intestine, CCK expression persisted from fetus to adulthood and was not influenced by IFN-γ. Intestinal cells expressing CCK did not co-express glucagon, suggesting that these cells are phenotypically distinct from CCK-expressing cells in the pancreatic islets, and the effect of IFN-γ on CCK varies depending upon the cytokine's specific microenvironment.",
author = "G. Liu and Pakala, {S. V.} and D. Gu and T. Krahl and L. Mocnik and N. Sarvetnick",
year = "2001",
month = "5",
day = "28",
doi = "10.1677/joe.0.1690233",
language = "English (US)",
volume = "169",
pages = "233--240",
journal = "Journal of Endocrinology",
issn = "0022-0795",
publisher = "Society for Endocrinology",
number = "2",

}

TY - JOUR

T1 - Cholecystokinin expression in the developing and regenerating pancreas and intestine

AU - Liu, G.

AU - Pakala, S. V.

AU - Gu, D.

AU - Krahl, T.

AU - Mocnik, L.

AU - Sarvetnick, N.

PY - 2001/5/28

Y1 - 2001/5/28

N2 - In developmental terms, the endocrine system of neither the gut nor the pancreatic islets has been characterized fully. Little is known about the involvement 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)-γ transgenic mice, which exhibit pancreatic regeneration, during embryonic development, the postnatal period and adulthood. We also questioned whether IFN-γ influences the expression of CCK. The results from embryonic day 16 showed that all three strains had CCK in the acinar region of pancreata, and specifically in α cells that also expressed glucagon. However, in adulthood only BALB/c and NOD mice continued this pattern. By contrast, in IFN-γ transgenic mice, CCK expression was suppressed from birth to 3 months of age in the pancreata but not intestines. However, by 5 months of age, CCK expression appeared in the regenerating pancreatic ductal region of IFN-γ transgenic mice. In the intestine, CCK expression persisted from fetus to adulthood and was not influenced by IFN-γ. Intestinal cells expressing CCK did not co-express glucagon, suggesting that these cells are phenotypically distinct from CCK-expressing cells in the pancreatic islets, and the effect of IFN-γ on CCK varies depending upon the cytokine's specific microenvironment.

AB - In developmental terms, the endocrine system of neither the gut nor the pancreatic islets has been characterized fully. Little is known about the involvement 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)-γ transgenic mice, which exhibit pancreatic regeneration, during embryonic development, the postnatal period and adulthood. We also questioned whether IFN-γ influences the expression of CCK. The results from embryonic day 16 showed that all three strains had CCK in the acinar region of pancreata, and specifically in α cells that also expressed glucagon. However, in adulthood only BALB/c and NOD mice continued this pattern. By contrast, in IFN-γ transgenic mice, CCK expression was suppressed from birth to 3 months of age in the pancreata but not intestines. However, by 5 months of age, CCK expression appeared in the regenerating pancreatic ductal region of IFN-γ transgenic mice. In the intestine, CCK expression persisted from fetus to adulthood and was not influenced by IFN-γ. Intestinal cells expressing CCK did not co-express glucagon, suggesting that these cells are phenotypically distinct from CCK-expressing cells in the pancreatic islets, and the effect of IFN-γ on CCK varies depending upon the cytokine's specific microenvironment.

UR - http://www.scopus.com/inward/record.url?scp=0035002915&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035002915&partnerID=8YFLogxK

U2 - 10.1677/joe.0.1690233

DO - 10.1677/joe.0.1690233

M3 - Article

C2 - 11312140

AN - SCOPUS:0035002915

VL - 169

SP - 233

EP - 240

JO - Journal of Endocrinology

JF - Journal of Endocrinology

SN - 0022-0795

IS - 2

ER -