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New perspectives on pancreatic islet glucokinase

New perspectives on pancreatic islet glucokinase INDIVIDUALS the blood sugar is maintained in an admirably narrow range both after a meal during fasting. When glucose is ingested, the pancreatic P-cells secrete insulin promptly, csequently the dispositi of glucose, primarily by the liver, curbs the blood glucose from rising to unphysiologicaevels. Hepatic glucose uptake is stimulated by the combined effects of hyperglycemia increased insulin ccentrati in the portal blood so that ly a fracti of the ingested glucose, a net value as little as 15% (23) possibly up to 75% (44), escapes from the splanchnic circulati into the peripheral circulati. Postabsorptively during more extended fasting, the other h, counterregulatory hormes prevent the blood glucose from falling to dangerously low levels by augmenting hepatic glycogenolysis gluceogenesis ( 1). In the present brief review we are ccerned with e narrow aspect of this complex system of feedback loops maintaining euglycemia, i.e., the biochemical basis of the glucostat functi of the pancreatic ,&cells, more precisely with the P-cell glucose sensor molecule “” (see the insert of 1). Because is also an important factor for hepatic glycogen storage glucose metabolism, our review will deal with selected pertinent informati liver . (ATP:D-glucose 6-phosphotransferase, 0193~1849/84 $1.50 Copyright 0 1984 the American http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

New perspectives on pancreatic islet glucokinase

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Publisher
The American Physiological Society
Copyright
Copyright © 1984 the American Physiological Society
ISSN
0193-1849
eISSN
1522-1555
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Abstract

INDIVIDUALS the blood sugar is maintained in an admirably narrow range both after a meal during fasting. When glucose is ingested, the pancreatic P-cells secrete insulin promptly, csequently the dispositi of glucose, primarily by the liver, curbs the blood glucose from rising to unphysiologicaevels. Hepatic glucose uptake is stimulated by the combined effects of hyperglycemia increased insulin ccentrati in the portal blood so that ly a fracti of the ingested glucose, a net value as little as 15% (23) possibly up to 75% (44), escapes from the splanchnic circulati into the peripheral circulati. Postabsorptively during more extended fasting, the other h, counterregulatory hormes prevent the blood glucose from falling to dangerously low levels by augmenting hepatic glycogenolysis gluceogenesis ( 1). In the present brief review we are ccerned with e narrow aspect of this complex system of feedback loops maintaining euglycemia, i.e., the biochemical basis of the glucostat functi of the pancreatic ,&cells, more precisely with the P-cell glucose sensor molecule “” (see the insert of 1). Because is also an important factor for hepatic glycogen storage glucose metabolism, our review will deal with selected pertinent informati liver . (ATP:D-glucose 6-phosphotransferase, 0193~1849/84 $1.50 Copyright 0 1984 the American

Journal

AJP - Endocrinology and Metabolism – The American Physiological Society

Published: Jan 1, 1984

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