The pancreatic β-cell recognition of insulin secretagogues. VIII. Comparisons of glucose with glyceraldehyde isomers and dihydroxyacetone
(1974) In Archives of Biochemistry and Biophysics 162(2). p.448-457- Abstract
d-Glyceraldehyde stimulated the release of insulin from pancreatic islets of Umeå- ob ob-mice whether or not glucose was present in the medium. Like the action of glucose, that of d-glyceraldehyde was biphasic in time, exhibited a sigmoidal dose-response relationship, was potentiated by theophylline, arginine, iodoacetamide, or l-glyceraldehyde, and was inhibited by epinephrine, 2,4-dinitrophenol, or Ca2+ deficiency. Half-maximum and maximum stimulations were produced by about 3 mm and 10 mm d-glyceraldehyde. Positive interactions were observed between 5 mm d-glyceraldehyde and 5 mm glucose and between 10 mm d-glyceraldehyde and 10 mm leucine. Mannoheptulose (10 mm) or glucosamine (10 mm) did not inhibit but potentiated the... (More)
d-Glyceraldehyde stimulated the release of insulin from pancreatic islets of Umeå- ob ob-mice whether or not glucose was present in the medium. Like the action of glucose, that of d-glyceraldehyde was biphasic in time, exhibited a sigmoidal dose-response relationship, was potentiated by theophylline, arginine, iodoacetamide, or l-glyceraldehyde, and was inhibited by epinephrine, 2,4-dinitrophenol, or Ca2+ deficiency. Half-maximum and maximum stimulations were produced by about 3 mm and 10 mm d-glyceraldehyde. Positive interactions were observed between 5 mm d-glyceraldehyde and 5 mm glucose and between 10 mm d-glyceraldehyde and 10 mm leucine. Mannoheptulose (10 mm) or glucosamine (10 mm) did not inhibit but potentiated the effect of 10 mm d-glyceraldehyde. Dihydroxyacetone (2.5-20 mm) also initiated insulin release in the absence of glucose. On the other hand, 5-10 mm l-glyceraldehyde did not initiate secretion but potentiated the effects of 5 mm glucose or 5 mm d-glyceraldehyde. d-Glyceraldehyde or dihydroxyacetone reduced the production of 14CO2 from d-[U-14C]glucose; l-glyceraldehyde had a smaller and statistically insignificant effect. The results suggest that by being phosphorylated and entering glycolysis in the β-cells, d-glyceraldehyde and dihydroxyacetone act as functional analogues of glucose as secretory stimulus. Initiation of insulin release by glucose, d-glyceraldehyde, or dihydroxyacetone may thus depend on the production of a metabolic signal at or below the triose phosphate level.
(Less)
- author
- Hellman, Bo ; Idahl, Lars Åke ; Lernmark, Åke LU ; Sehlin, Janove and Täljedal, Inge Bert
- publishing date
- 1974-01-01
- type
- Contribution to journal
- publication status
- published
- in
- Archives of Biochemistry and Biophysics
- volume
- 162
- issue
- 2
- pages
- 10 pages
- publisher
- Academic Press
- external identifiers
-
- pmid:4210076
- scopus:0016192841
- ISSN
- 0003-9861
- DOI
- 10.1016/0003-9861(74)90204-5
- language
- English
- LU publication?
- no
- id
- 1975c277-73d2-46b2-9a9b-e470d0936af6
- date added to LUP
- 2019-09-18 12:17:46
- date last changed
- 2024-03-13 08:12:30
@article{1975c277-73d2-46b2-9a9b-e470d0936af6, abstract = {{<p>d-Glyceraldehyde stimulated the release of insulin from pancreatic islets of Umeå- ob ob-mice whether or not glucose was present in the medium. Like the action of glucose, that of d-glyceraldehyde was biphasic in time, exhibited a sigmoidal dose-response relationship, was potentiated by theophylline, arginine, iodoacetamide, or l-glyceraldehyde, and was inhibited by epinephrine, 2,4-dinitrophenol, or Ca<sup>2+</sup> deficiency. Half-maximum and maximum stimulations were produced by about 3 mm and 10 mm d-glyceraldehyde. Positive interactions were observed between 5 mm d-glyceraldehyde and 5 mm glucose and between 10 mm d-glyceraldehyde and 10 mm leucine. Mannoheptulose (10 mm) or glucosamine (10 mm) did not inhibit but potentiated the effect of 10 mm d-glyceraldehyde. Dihydroxyacetone (2.5-20 mm) also initiated insulin release in the absence of glucose. On the other hand, 5-10 mm l-glyceraldehyde did not initiate secretion but potentiated the effects of 5 mm glucose or 5 mm d-glyceraldehyde. d-Glyceraldehyde or dihydroxyacetone reduced the production of <sup>14</sup>CO<sub>2</sub> from d-[U-<sup>14</sup>C]glucose; l-glyceraldehyde had a smaller and statistically insignificant effect. The results suggest that by being phosphorylated and entering glycolysis in the β-cells, d-glyceraldehyde and dihydroxyacetone act as functional analogues of glucose as secretory stimulus. Initiation of insulin release by glucose, d-glyceraldehyde, or dihydroxyacetone may thus depend on the production of a metabolic signal at or below the triose phosphate level.</p>}}, author = {{Hellman, Bo and Idahl, Lars Åke and Lernmark, Åke and Sehlin, Janove and Täljedal, Inge Bert}}, issn = {{0003-9861}}, language = {{eng}}, month = {{01}}, number = {{2}}, pages = {{448--457}}, publisher = {{Academic Press}}, series = {{Archives of Biochemistry and Biophysics}}, title = {{The pancreatic β-cell recognition of insulin secretagogues. VIII. Comparisons of glucose with glyceraldehyde isomers and dihydroxyacetone}}, url = {{http://dx.doi.org/10.1016/0003-9861(74)90204-5}}, doi = {{10.1016/0003-9861(74)90204-5}}, volume = {{162}}, year = {{1974}}, }