Abstract
C-peptide, a cleavage product from the processing of proinsulin to insulin, has been considered to possess little if any biological activity other than its participation in insulin synthesis. Injection of human C-peptide prevented or attenuated vascular and neural (electrophysiological) dysfunction and impaired Na+- and K+-dependent adenosine triphosphate activity in tissues of diabetic rats. Nonpolar amino acids in the midportion of the peptide were required for these biological effects. Synthetic reverse sequence (retro) and all-D-amino acid (enantio) C-peptides were equipotent to native C-peptide, which indicates that the effects of C-peptide on diabetic vascular and neural dysfunction were mediated by nonchiral interactions instead of stereospecific receptors or binding sites.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Blood Circulation / drug effects
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Blood Glucose / metabolism
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C-Peptide / chemistry*
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C-Peptide / pharmacology
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C-Peptide / therapeutic use*
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Capillary Permeability / drug effects
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Circular Dichroism
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Diabetes Mellitus, Experimental / drug therapy
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Diabetes Mellitus, Experimental / physiopathology
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Diabetic Angiopathies / prevention & control*
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Diabetic Neuropathies / prevention & control*
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Humans
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Male
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Molecular Sequence Data
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Neural Conduction / drug effects
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Peptide Fragments / pharmacology
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Protein Structure, Secondary
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Rats
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Rats, Sprague-Dawley
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Sodium-Potassium-Exchanging ATPase / metabolism
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Stereoisomerism
Substances
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Blood Glucose
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C-Peptide
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Peptide Fragments
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Sodium-Potassium-Exchanging ATPase