Abstract
In certain non-insulin-dependent diabetic patients, the secretory capacity of the pancreatic B-cell appears to be more severely affected in response to stimulation by D-glucose than other secretagogues [1]. Since D-glucose represents a major, albeit not the sole, regulator of insulin release under physiological conditions [2], the mechanisms possibly responsible for impaired recognition of this hexose by islet cells are directly relevant to our understanding of the pathology of the endocrine pancreas in diabetes mellitus.
This work was supported, in part, by grants from the Belgian Foundation for Scientific Medical Research and the NATO Scientific Affairs Division.
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Malaisse, W.J. (1988). Possible Sites for Deficient Glucose Recognition in Islet Cells. In: Lefèbvre, P.J., Pipeleers, D.G. (eds) The Pathology of the Endocrine Pancreas in Diabetes. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72691-0_12
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DOI: https://doi.org/10.1007/978-3-642-72691-0_12
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