Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

The pancreatic β cell recognition of insulin secretagogues. XII. Insulin release in response to halogenated hexosamines

Hellman, B. ; Idahl, L. A. ; Lernmark, A. LU orcid ; Täljedal, I. B. and Thomas, E. W. (1976) In Molecular Pharmacology 12(2). p.208-216
Abstract

The effects of N iodoacetyl 2 amino 2 deoxy (D) glucose and various N bromoacetylglycosylamines on the release of insulin from microdissected pancreatic islets of non inbred ob/ob mice were studied. N Bromoacetyl β (D) glucosylamine (10 m(M)) initiated insulin release in the absence of (D) glucose and, at concentrations of 2.5-10 m(M), but not 20 m(M), potentiated insulin release in response to 10 m(M) (D) glucose. The potentiating, but not the initiating, action was significantly inhibited in the presence of mannoheptulose. N Bromoacetyl β (L) glucosylamine or N bromoacetyl β (D) galactosylamine had no effect in the absence of (D) glucose. However, 2.5-20 m(M) concentrations of the (L) glucose derivative and 1.25-5.0 m(M)... (More)

The effects of N iodoacetyl 2 amino 2 deoxy (D) glucose and various N bromoacetylglycosylamines on the release of insulin from microdissected pancreatic islets of non inbred ob/ob mice were studied. N Bromoacetyl β (D) glucosylamine (10 m(M)) initiated insulin release in the absence of (D) glucose and, at concentrations of 2.5-10 m(M), but not 20 m(M), potentiated insulin release in response to 10 m(M) (D) glucose. The potentiating, but not the initiating, action was significantly inhibited in the presence of mannoheptulose. N Bromoacetyl β (L) glucosylamine or N bromoacetyl β (D) galactosylamine had no effect in the absence of (D) glucose. However, 2.5-20 m(M) concentrations of the (L) glucose derivative and 1.25-5.0 m(M) concentrations of the (D) galactose derivative potentiated the effect of 10 m(M) (D) glucose; at 20 m(M) the (D) galactose derivative inhibited the (D) glucose induced insulin release. N Iodoacetyl 2 amino 2 deoxy (D) glucose (0.1-10 m(M)) did not initiate or potentiate insulin release but, at a concentration of 10 m(M), inhibited the effect of (D) glucose. The results support this hypothesis that alkylation of thiol groups in the β cell plasma membrane leads to potentiation of (D) glucose induced insulin release if glycolysis is not simultaneously inhibited by the thiol reagent. If a regulatory site ('direct receptor') for the (D) glucose molecule plays a role in stimulus recognition, N iodoacetyl 2 amino 2 deoxy (D) glucose may be valuable in attempts to label and isolate it.

(Less)
Please use this url to cite or link to this publication:
author
; ; ; and
publishing date
type
Contribution to journal
publication status
published
in
Molecular Pharmacology
volume
12
issue
2
pages
9 pages
publisher
American Society for Pharmacology and Experimental Therapeutics
external identifiers
  • scopus:0017236695
  • pmid:772418
ISSN
0026-895X
language
English
LU publication?
no
id
93931cad-e94a-4eea-9b49-467544ac8311
date added to LUP
2019-09-18 12:11:51
date last changed
2024-03-13 08:12:05
@article{93931cad-e94a-4eea-9b49-467544ac8311,
  abstract     = {{<p>The effects of N iodoacetyl 2 amino 2 deoxy (D) glucose and various N bromoacetylglycosylamines on the release of insulin from microdissected pancreatic islets of non inbred ob/ob mice were studied. N Bromoacetyl β (D) glucosylamine (10 m(M)) initiated insulin release in the absence of (D) glucose and, at concentrations of 2.5-10 m(M), but not 20 m(M), potentiated insulin release in response to 10 m(M) (D) glucose. The potentiating, but not the initiating, action was significantly inhibited in the presence of mannoheptulose. N Bromoacetyl β (L) glucosylamine or N bromoacetyl β (D) galactosylamine had no effect in the absence of (D) glucose. However, 2.5-20 m(M) concentrations of the (L) glucose derivative and 1.25-5.0 m(M) concentrations of the (D) galactose derivative potentiated the effect of 10 m(M) (D) glucose; at 20 m(M) the (D) galactose derivative inhibited the (D) glucose induced insulin release. N Iodoacetyl 2 amino 2 deoxy (D) glucose (0.1-10 m(M)) did not initiate or potentiate insulin release but, at a concentration of 10 m(M), inhibited the effect of (D) glucose. The results support this hypothesis that alkylation of thiol groups in the β cell plasma membrane leads to potentiation of (D) glucose induced insulin release if glycolysis is not simultaneously inhibited by the thiol reagent. If a regulatory site ('direct receptor') for the (D) glucose molecule plays a role in stimulus recognition, N iodoacetyl 2 amino 2 deoxy (D) glucose may be valuable in attempts to label and isolate it.</p>}},
  author       = {{Hellman, B. and Idahl, L. A. and Lernmark, A. and Täljedal, I. B. and Thomas, E. W.}},
  issn         = {{0026-895X}},
  language     = {{eng}},
  month        = {{12}},
  number       = {{2}},
  pages        = {{208--216}},
  publisher    = {{American Society for Pharmacology and Experimental Therapeutics}},
  series       = {{Molecular Pharmacology}},
  title        = {{The pancreatic β cell recognition of insulin secretagogues. XII. Insulin release in response to halogenated hexosamines}},
  volume       = {{12}},
  year         = {{1976}},
}