Elsewhere we have proposed that the rapid transient efflux of 32P orthophosphate that occurs when prelabeled pancreatic islets are exposed to nutrient secretagogues (the “phosphate flush”) reflects one of the earliest steps in islet stimulus-secretion coupling. We have now shown that the “phosphate flush” is much smaller with islets from fetal rats 21½ days old. This could be attributed to decreased cellular stores of radioactivity, especially inorganic orthophosphate (32P), at the onset of stimulation, which may have been due, in part, to the diminished ability of fetal islets to retain the radiophosphorus accumulated during the labeling period. Certain other differences in phosphate metabolism were also observed. With prelabeled islets from adult rats, exposure to 3.0 mg. per milliliter glucose effected acute increases in the tissue content of AT32P and GT32P. Comparable stimulation of prelabeled fetal islets with 3.0 mg. per milliliter glucose did not elicit detectable changes in the labeling of ATP or GTP. The findings indicate that selected aspects of phosphate metabolism may be immature in fetal islets and, perhaps, implicated in their obtunded secretion of insulin in response to stimulation with glucose.
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Original Contributions| June 01 1978
Phosphate Metabolism and Glucose-initiated Efflux of Phosphate Ions in Islets of Fetal Pancreas
Kjell Asplund, MD;
Reprint requests should be addressed: Dr. Norbert Freinkel, 303 East Chicago Avenue, Chicago, Illinois 60611.
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Kjell Asplund, Norbert Freinkel; Phosphate Metabolism and Glucose-initiated Efflux of Phosphate Ions in Islets of Fetal Pancreas. Diabetes 1 June 1978; 27 (6): 611–619. https://doi.org/10.2337/diab.27.6.611
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