The pancreatic β-cell recognition of insulin secretagogues. Comparisons of glucose with glyceraldehyde isomers and dihydroxyacetone

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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.


  • Bo Hellman
  • Lars Åke Idahl
  • Åke Lernmark
  • Janove Sehlin
  • Inge Bert Täljedal
External organisations
  • Umeå University
Original languageEnglish
Pages (from-to)448-457
Number of pages10
JournalArchives of Biochemistry and Biophysics
Issue number2
Publication statusPublished - 1974 Jan 1
Publication categoryResearch
Externally publishedYes