Deficiency of Ascorbic Acid in Experimental Diabetes: Relationship With Collagen and Polyol Pathway Abnormalities | Zendy

Susan V. McLennan | Zendy; Dennis K. Yue | Zendy; Elizabeth Fisher | Zendy; C. Capogreco | Zendy; Scott Heffernan | Zendy; Glynis R Ross | Zendy; John R. Turtle | Zendy

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Deficiency of Ascorbic Acid in Experimental Diabetes: Relationship With Collagen and Polyol Pathway Abnormalities

Author(s) -

Susan V. McLennan,

Dennis K. Yue,

Elizabeth Fisher,

C. Capogreco,

Scott Heffernan,

Glynis R Ross,

John R. Turtle

Publication year - 1988

Publication title -

diabetes

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.219

H-Index - 330

eISSN - 1939-327X

pISSN - 0012-1797

DOI - 10.2337/diab.37.3.359

Subject(s) - ascorbic acid , aldose reductase , polyol pathway , aldose reductase inhibitor , medicine , endocrinology , diabetes mellitus , chemistry , granulation tissue , enzyme , sorbitol , biochemistry , wound healing , surgery , food science

The plasma and tissue concentration of ascorbic acid (AA) is reduced in diabetes. This study was designed to investigate the mechanism and significance of this phenomenon. The low plasma AA concentration of diabetic rats can be normalized by dietary AA supplement (20-40 mg/day), a dosage approximately equal to the maximal synthetic rate of this substance in the rats. Treatment of diabetic rats with this regime prevented the decrease in activity of granulation tissue prolyl hydroxylase (PRLase), an AA-dependent enzyme required for maintaining the normal properties of collagen. The decreased plasma AA concentration and granulation tissue PRLase activity in diabetes can also be normalized by the aldose reductase inhibitor tolrestat. We conclude that in diabetic animals there is a true deficiency of AA that may be responsible for some of the changes of collagen observed in diabetes. Treatment with AA or an aldose reductase inhibitor may prevent some of the diabetic complications with underlying collagen abnormalities.

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