The pancreatic β cell recognition of insulin secretagogues. XII. Insulin release in response to halogenated hexosamines
(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)
- author
- Hellman, B. ; Idahl, L. A. ; Lernmark, A. LU ; Täljedal, I. B. and Thomas, E. W.
- publishing date
- 1976-12-01
- 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}}, }