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Metabolic and insulin-releasing activities of D-glucose anomers

Naturevolume 254pages7577 (1975) | Download Citation



GRODSKY et al.1 proposed that glucose stimulates insulin secretion because the sugar is metabolised in the pancreatic β cells; this view of stimulus recognition was later termed the substrate–site hypothesis2. The hypothesis has received support from observed correlations between rates of insulin release and various parameters of glucose metabolism in the pancreatic islets. It is particularly striking that a triose, D-glyceraldehyde, has been shown to mimic the electrophysiological3 and insulin-releasing4–6 actions of glucose; D-glyceraldehyde is oxidised and dilutes 14CO2 arising from D-(U-14C)-glucose in the islets4–6. Although the substrate–site hypothesis has been criticised (for example, refs 7 and 8), many of the arguments raised may be doubtful for reasons discussed elsewhere9. An important challenge to the hypothesis is the observation that the α anomer of D-glucose is more effective than the β anomer in stimulating insulin secretion10,11. For the anomeric specificity of the D-glucose recognition system to stand up as evidence against the substrate–site hypothesis, however, it must be shown that the transport, phosphorylation or further metabolism of glucose does not exhibit the same anomeric specificity in the β cell. We report here that β-D-glucose is at least as effective as α-D-glucose in stimulating counter-transport of 3-O-methyl-D-glucose, increasing the islet content of glucose-6-phosphate, and diluting 3H2O that results from the metabolism of D-(5-3H)-glucose.

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  1. Department of Histology, University of Umea, S-901 87, Umea, Sweden

    • L-Å. IDAHL
    • , J. SEHLIN
    •  & I-B. TALJEDAL


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