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Molecular Pharmacology

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Research ArticleArticle

Molecular Requirements for Recognition at a Glucoreceptor for Insulin Release

DANIEL C. WEAVER, C. DAVID BARRY, MICHAEL L. MCDANIEL, GARLAND R. MARSHALL and PAUL E. LACY
Molecular Pharmacology September 1979, 16 (2) 361-368;
DANIEL C. WEAVER
Department of Pathology Computer Systems Laboratory, and Department of Physiology and Biophysics, Washington University, St. Louis, Mo.
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C. DAVID BARRY
Department of Pathology Computer Systems Laboratory, and Department of Physiology and Biophysics, Washington University, St. Louis, Mo.
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MICHAEL L. MCDANIEL
Department of Pathology Computer Systems Laboratory, and Department of Physiology and Biophysics, Washington University, St. Louis, Mo.
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GARLAND R. MARSHALL
Department of Pathology Computer Systems Laboratory, and Department of Physiology and Biophysics, Washington University, St. Louis, Mo.
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PAUL E. LACY
Department of Pathology Computer Systems Laboratory, and Department of Physiology and Biophysics, Washington University, St. Louis, Mo.
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Abstract

Alloxan and ninhydrin affect insulin release by first stimulation and then inhibition of subsequent glucose-induced insulin release from the β-cells in the islets of Langerhans. The structures of D-glucose and D-mannose, the two hexoses that protect against them and initiate insulin release, were analyzed and found to share with alloxan and ninhydrin common molecular properties. These common molecular properties were: An oxygen at C(1); a hydroxyl at C(2), either axial or equatorial; an equatorial oxygen at C(3); and at position 5 an electron density. Further structural analysis revealed that alloxan and ninhydrin would require little, if any, additional volume than that required for recognition of the active hexoses, D-glucose and D-mannose at a common site. Other hexoses (1-deoxy-D-glucose, 2-deoxy-D-glucose, D-allose, D-galactose, lyxose, xylose, 6-deoxy-D-glucose, and L-glucose) which either did not protect against alloxan and ninhydrin or did not initiate insulin release were found to vary in their structure from the active hexoses. Based on the presently available evidence, a hypothesis was advanced that alloxan, ninhydrin, and the active hexoses interact at a common receptor to initiate the first phase of insulin release.

ACKNOWLEDGMENTS We wish to thank C. A. Bry, C. J. Fink and R. W. Homer for their excellent technical assistance.

  • Copyright © 1979 by Academic Press, Inc.

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Molecular Pharmacology
Vol. 16, Issue 2
1 Sep 1979
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Research ArticleArticle

Molecular Requirements for Recognition at a Glucoreceptor for Insulin Release

DANIEL C. WEAVER, C. DAVID BARRY, MICHAEL L. MCDANIEL, GARLAND R. MARSHALL and PAUL E. LACY
Molecular Pharmacology September 1, 1979, 16 (2) 361-368;

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Research ArticleArticle

Molecular Requirements for Recognition at a Glucoreceptor for Insulin Release

DANIEL C. WEAVER, C. DAVID BARRY, MICHAEL L. MCDANIEL, GARLAND R. MARSHALL and PAUL E. LACY
Molecular Pharmacology September 1, 1979, 16 (2) 361-368;
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