Amylin modulates β-cell glucose sensing via effects on stimulus-secretion coupling

P. Kay Wagoner, Chen Chen, Jennings F. Worley, Iain D. Dukes, Gerry S. Oxford

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

The release of insulin from the pancreatic β cell is dependent upon a complex interplay between stimulators and inhibitors. Recently, amylin, a peptide secreted by pancreatic β cells, has been implicated in the development of type II (noninsulin dependent) diabetes through its modulation of the peripheral effects of insulin. However, the effect of amylin on insulin secretion from the β cell has remained controversial. It is reported here that in single β cells exhibiting normal glucose sensing, amylin causes membrane hyperpolarization, increases in net outward current, and reductions in insulin secretion. In contrast, in cells with abnormal glucose sensing (e.g., from db/db diabetic mice), amylin has no effect on electrical activity or secretion. Thus, amylin's effects on excitation-secretion coupling in the β cell of the pancreas appear to be linked to the cell's capacity for normal glucose sensing.

Original languageEnglish (US)
Pages (from-to)9145-9149
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume90
Issue number19
StatePublished - Oct 1 1993
Externally publishedYes

Fingerprint

Islet Amyloid Polypeptide
Glucose
Insulin
Pancreas
Peptides
Membranes

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

Amylin modulates β-cell glucose sensing via effects on stimulus-secretion coupling. / Wagoner, P. Kay; Chen, Chen; Worley, Jennings F.; Dukes, Iain D.; Oxford, Gerry S.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 90, No. 19, 01.10.1993, p. 9145-9149.

Research output: Contribution to journalArticle

Wagoner, P. Kay ; Chen, Chen ; Worley, Jennings F. ; Dukes, Iain D. ; Oxford, Gerry S. / Amylin modulates β-cell glucose sensing via effects on stimulus-secretion coupling. In: Proceedings of the National Academy of Sciences of the United States of America. 1993 ; Vol. 90, No. 19. pp. 9145-9149.
@article{67e45b076ef843a7a228afbbd04c61be,
title = "Amylin modulates β-cell glucose sensing via effects on stimulus-secretion coupling",
abstract = "The release of insulin from the pancreatic β cell is dependent upon a complex interplay between stimulators and inhibitors. Recently, amylin, a peptide secreted by pancreatic β cells, has been implicated in the development of type II (noninsulin dependent) diabetes through its modulation of the peripheral effects of insulin. However, the effect of amylin on insulin secretion from the β cell has remained controversial. It is reported here that in single β cells exhibiting normal glucose sensing, amylin causes membrane hyperpolarization, increases in net outward current, and reductions in insulin secretion. In contrast, in cells with abnormal glucose sensing (e.g., from db/db diabetic mice), amylin has no effect on electrical activity or secretion. Thus, amylin's effects on excitation-secretion coupling in the β cell of the pancreas appear to be linked to the cell's capacity for normal glucose sensing.",
author = "Wagoner, {P. Kay} and Chen Chen and Worley, {Jennings F.} and Dukes, {Iain D.} and Oxford, {Gerry S.}",
year = "1993",
month = "10",
day = "1",
language = "English (US)",
volume = "90",
pages = "9145--9149",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "19",

}

TY - JOUR

T1 - Amylin modulates β-cell glucose sensing via effects on stimulus-secretion coupling

AU - Wagoner, P. Kay

AU - Chen, Chen

AU - Worley, Jennings F.

AU - Dukes, Iain D.

AU - Oxford, Gerry S.

PY - 1993/10/1

Y1 - 1993/10/1

N2 - The release of insulin from the pancreatic β cell is dependent upon a complex interplay between stimulators and inhibitors. Recently, amylin, a peptide secreted by pancreatic β cells, has been implicated in the development of type II (noninsulin dependent) diabetes through its modulation of the peripheral effects of insulin. However, the effect of amylin on insulin secretion from the β cell has remained controversial. It is reported here that in single β cells exhibiting normal glucose sensing, amylin causes membrane hyperpolarization, increases in net outward current, and reductions in insulin secretion. In contrast, in cells with abnormal glucose sensing (e.g., from db/db diabetic mice), amylin has no effect on electrical activity or secretion. Thus, amylin's effects on excitation-secretion coupling in the β cell of the pancreas appear to be linked to the cell's capacity for normal glucose sensing.

AB - The release of insulin from the pancreatic β cell is dependent upon a complex interplay between stimulators and inhibitors. Recently, amylin, a peptide secreted by pancreatic β cells, has been implicated in the development of type II (noninsulin dependent) diabetes through its modulation of the peripheral effects of insulin. However, the effect of amylin on insulin secretion from the β cell has remained controversial. It is reported here that in single β cells exhibiting normal glucose sensing, amylin causes membrane hyperpolarization, increases in net outward current, and reductions in insulin secretion. In contrast, in cells with abnormal glucose sensing (e.g., from db/db diabetic mice), amylin has no effect on electrical activity or secretion. Thus, amylin's effects on excitation-secretion coupling in the β cell of the pancreas appear to be linked to the cell's capacity for normal glucose sensing.

UR - http://www.scopus.com/inward/record.url?scp=0027449254&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027449254&partnerID=8YFLogxK

M3 - Article

C2 - 8415669

AN - SCOPUS:0027449254

VL - 90

SP - 9145

EP - 9149

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 19

ER -