Environmental modulation of the inhibitory action of D-mannoheptulose upon D-glucose metabolism in isolated rat pancreatic islets

In pancreatic islets prepared from fed rats and incubated at a low concentration (1·7 mM) of D‐glucose, D‐mannoheptulose (10·0 mM) virtually fails to affect the metabolism of the hexose. Likewise, in islets from starved rats, the relative extent of the inhibitory action of D‐mannoheptulose upon D‐gl...

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Veröffentlicht in:Cell biochemistry and function 1999-03, Vol.17 (1), p.65-71
Hauptverfasser: Picton, Sally, Malaisse, Willy J.
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Sprache:eng
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Zusammenfassung:In pancreatic islets prepared from fed rats and incubated at a low concentration (1·7 mM) of D‐glucose, D‐mannoheptulose (10·0 mM) virtually fails to affect the metabolism of the hexose. Likewise, in islets from starved rats, the relative extent of the inhibitory action of D‐mannoheptulose upon D‐glucose metabolism is much more marked at high (16·7 mM) than low (1·7 mM) hexose concentration. Nevertheless, despite decreasing the metabolism of D‐glucose, starvation augments the sensitivity to D‐mannoheptulose in the islets incubated at a low concentration of the hexose. D‐galactose, but not D‐fructose, also augments the inhibitory action of D‐mannoheptulose upon D‐glucose metabolism in islets prepared from fed rats and exposed to the low concentration of D‐glucose. A comparable situation prevails in islets exposed to 2‐ketoisocaproate. Forskolin, however, which decreases D‐glucose catabolism in the islets from fed rats exposed to 1·7 mM D‐glucose, fails to affect significantly the inhibitory action of D‐mannoheptulose on D‐glucose metabolism. It is proposed that hexoses transported by the same carrier as D‐glucose and non‐glucidic nutrient secretagogues somehow increase D‐mannoheptulose uptake by the islet cells. The latter two conditions may be operative in islets exposed to a high concentration of D‐glucose, this accounting for the exquisite sensitivity to D‐mannoheptulose of glucose‐stimulated islets. Copyright © 1999 John Wiley & Sons, Ltd.
ISSN:0263-6484
1099-0844
DOI:10.1002/(SICI)1099-0844(199903)17:1<65::AID-CBF812>3.0.CO;2-T