Islet cell hormones and chronic pancreatitis

Shawn P. Fagan, Dana Andersen, F. Charles Brunicardi

Research output: Contribution to journalArticle

Abstract

Many of the pathophysiologic responses observed in chronic pancreatitis are related in part to disruption of the insulo-acinar axis, to destruction of islet cell mass, or to both. Each of the four types of hormone-secreting beta cells is affected by the destructive process of chronic pancreatitis. The insulin-secreting beta cells appear to be affected in both a qualitative and quantitative manner. Directly related to the changes in the beta cell are the physiologic responses of the glucagon-secreting alpha cells. Their physiologic response in chronic pancreatitis appears to be related to the residual beta cell function. Recently, pancreatic polypeptide has been implicated as a contributor to the abnormal glucose metabolism in pancreatogenic diabetes. The deficiency of this peptide appears to influence the expression of hepatocyte insulin receptors in chronic pancreatitis. There also appears to be a close correlation between the degree of PP secretion deficiency and pancreatic exocrine insufficiency. Although somatostatin appears to have an important role in the insulo-acinar axis, the effects of chronic pancreatitis on the function of somatostatin in the insulo-acinar axis are poorly understood. There is a need for further exploration of the interrelation of the endocrine and the exocrine pancreas to develop better treatment options for the alterations in glucose metabolism that occur in chronic pancreatitis.

Original languageEnglish (US)
Pages (from-to)7-16
Number of pages10
JournalProblems in General Surgery
Volume15
Issue number1
StatePublished - 1998
Externally publishedYes

Fingerprint

Chronic Pancreatitis
Islets of Langerhans
Hormones
Somatostatin
Glucagon-Secreting Cells
Exocrine Pancreatic Insufficiency
Pancreatic Polypeptide
Glucose
Exocrine Pancreas
Insulin Receptor
Insulin-Secreting Cells
Hepatocytes
Peptides

ASJC Scopus subject areas

  • Surgery

Cite this

Fagan, S. P., Andersen, D., & Brunicardi, F. C. (1998). Islet cell hormones and chronic pancreatitis. Problems in General Surgery, 15(1), 7-16.

Islet cell hormones and chronic pancreatitis. / Fagan, Shawn P.; Andersen, Dana; Brunicardi, F. Charles.

In: Problems in General Surgery, Vol. 15, No. 1, 1998, p. 7-16.

Research output: Contribution to journalArticle

Fagan, SP, Andersen, D & Brunicardi, FC 1998, 'Islet cell hormones and chronic pancreatitis', Problems in General Surgery, vol. 15, no. 1, pp. 7-16.
Fagan, Shawn P. ; Andersen, Dana ; Brunicardi, F. Charles. / Islet cell hormones and chronic pancreatitis. In: Problems in General Surgery. 1998 ; Vol. 15, No. 1. pp. 7-16.
@article{56728a47de564b948a8eb9b5fc0c708a,
title = "Islet cell hormones and chronic pancreatitis",
abstract = "Many of the pathophysiologic responses observed in chronic pancreatitis are related in part to disruption of the insulo-acinar axis, to destruction of islet cell mass, or to both. Each of the four types of hormone-secreting beta cells is affected by the destructive process of chronic pancreatitis. The insulin-secreting beta cells appear to be affected in both a qualitative and quantitative manner. Directly related to the changes in the beta cell are the physiologic responses of the glucagon-secreting alpha cells. Their physiologic response in chronic pancreatitis appears to be related to the residual beta cell function. Recently, pancreatic polypeptide has been implicated as a contributor to the abnormal glucose metabolism in pancreatogenic diabetes. The deficiency of this peptide appears to influence the expression of hepatocyte insulin receptors in chronic pancreatitis. There also appears to be a close correlation between the degree of PP secretion deficiency and pancreatic exocrine insufficiency. Although somatostatin appears to have an important role in the insulo-acinar axis, the effects of chronic pancreatitis on the function of somatostatin in the insulo-acinar axis are poorly understood. There is a need for further exploration of the interrelation of the endocrine and the exocrine pancreas to develop better treatment options for the alterations in glucose metabolism that occur in chronic pancreatitis.",
author = "Fagan, {Shawn P.} and Dana Andersen and Brunicardi, {F. Charles}",
year = "1998",
language = "English (US)",
volume = "15",
pages = "7--16",
journal = "Problems in General Surgery",
issn = "0739-8328",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Islet cell hormones and chronic pancreatitis

AU - Fagan, Shawn P.

AU - Andersen, Dana

AU - Brunicardi, F. Charles

PY - 1998

Y1 - 1998

N2 - Many of the pathophysiologic responses observed in chronic pancreatitis are related in part to disruption of the insulo-acinar axis, to destruction of islet cell mass, or to both. Each of the four types of hormone-secreting beta cells is affected by the destructive process of chronic pancreatitis. The insulin-secreting beta cells appear to be affected in both a qualitative and quantitative manner. Directly related to the changes in the beta cell are the physiologic responses of the glucagon-secreting alpha cells. Their physiologic response in chronic pancreatitis appears to be related to the residual beta cell function. Recently, pancreatic polypeptide has been implicated as a contributor to the abnormal glucose metabolism in pancreatogenic diabetes. The deficiency of this peptide appears to influence the expression of hepatocyte insulin receptors in chronic pancreatitis. There also appears to be a close correlation between the degree of PP secretion deficiency and pancreatic exocrine insufficiency. Although somatostatin appears to have an important role in the insulo-acinar axis, the effects of chronic pancreatitis on the function of somatostatin in the insulo-acinar axis are poorly understood. There is a need for further exploration of the interrelation of the endocrine and the exocrine pancreas to develop better treatment options for the alterations in glucose metabolism that occur in chronic pancreatitis.

AB - Many of the pathophysiologic responses observed in chronic pancreatitis are related in part to disruption of the insulo-acinar axis, to destruction of islet cell mass, or to both. Each of the four types of hormone-secreting beta cells is affected by the destructive process of chronic pancreatitis. The insulin-secreting beta cells appear to be affected in both a qualitative and quantitative manner. Directly related to the changes in the beta cell are the physiologic responses of the glucagon-secreting alpha cells. Their physiologic response in chronic pancreatitis appears to be related to the residual beta cell function. Recently, pancreatic polypeptide has been implicated as a contributor to the abnormal glucose metabolism in pancreatogenic diabetes. The deficiency of this peptide appears to influence the expression of hepatocyte insulin receptors in chronic pancreatitis. There also appears to be a close correlation between the degree of PP secretion deficiency and pancreatic exocrine insufficiency. Although somatostatin appears to have an important role in the insulo-acinar axis, the effects of chronic pancreatitis on the function of somatostatin in the insulo-acinar axis are poorly understood. There is a need for further exploration of the interrelation of the endocrine and the exocrine pancreas to develop better treatment options for the alterations in glucose metabolism that occur in chronic pancreatitis.

UR - http://www.scopus.com/inward/record.url?scp=0031922435&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031922435&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0031922435

VL - 15

SP - 7

EP - 16

JO - Problems in General Surgery

JF - Problems in General Surgery

SN - 0739-8328

IS - 1

ER -