Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts

Guillermo Gomez, Courtney Townsend, D. W. Green, S. Rajaraman, G. H. Greeley, J. C. Thompson

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 ± 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 ± 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were comletely reversed by the simultaneous administration of CCK-8 (3 μg/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 ± 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume259
Issue number1 22-1
StatePublished - 1990

Fingerprint

Cholecystokinin
Bile Acids and Salts
Cholestyramine Resin
Growth
Taurocholic Acid
Devazepide
RNA
Cholecystokinin Receptors
Diet
DNA
Pancreas
Proteins

Keywords

  • cholestyramine
  • L365,718
  • sodium taurocholate

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts. / Gomez, Guillermo; Townsend, Courtney; Green, D. W.; Rajaraman, S.; Greeley, G. H.; Thompson, J. C.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 259, No. 1 22-1, 1990.

Research output: Contribution to journalArticle

Gomez, Guillermo ; Townsend, Courtney ; Green, D. W. ; Rajaraman, S. ; Greeley, G. H. ; Thompson, J. C. / Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts. In: American Journal of Physiology - Gastrointestinal and Liver Physiology. 1990 ; Vol. 259, No. 1 22-1.
@article{c58c10fe4f9840538ba046aa6db745ac,
title = "Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts",
abstract = "The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 ± 1.5 pM. Feeding mice a 0.5{\%} (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 ± 0.5 pM and decreased the total contents of pancreatic DNA by 22{\%}, RNA by 25{\%}, and protein by 24{\%}. All of the inhibitory effects of taurocholate on pancreatic growth were comletely reversed by the simultaneous administration of CCK-8 (3 μg/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4{\%} (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 ± 1.5 pM and increased the total contents of pancreatic DNA by 34{\%}, RNA by 40{\%}, and protein by 35{\%}. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.",
keywords = "cholestyramine, L365,718, sodium taurocholate",
author = "Guillermo Gomez and Courtney Townsend and Green, {D. W.} and S. Rajaraman and Greeley, {G. H.} and Thompson, {J. C.}",
year = "1990",
language = "English (US)",
volume = "259",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "1 22-1",

}

TY - JOUR

T1 - Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts

AU - Gomez, Guillermo

AU - Townsend, Courtney

AU - Green, D. W.

AU - Rajaraman, S.

AU - Greeley, G. H.

AU - Thompson, J. C.

PY - 1990

Y1 - 1990

N2 - The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 ± 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 ± 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were comletely reversed by the simultaneous administration of CCK-8 (3 μg/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 ± 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.

AB - The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 ± 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 ± 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were comletely reversed by the simultaneous administration of CCK-8 (3 μg/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 ± 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.

KW - cholestyramine

KW - L365,718

KW - sodium taurocholate

UR - http://www.scopus.com/inward/record.url?scp=0025363358&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025363358&partnerID=8YFLogxK

M3 - Article

C2 - 1695489

AN - SCOPUS:0025363358

VL - 259

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 1 22-1

ER -