Horm Metab Res 1993; 25(2): 82-87
DOI: 10.1055/s-2007-1002048
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© Georg Thieme Verlag, Stuttgart · New York

Apolipoprotein E Metabolism in Sciatic Nerves of Diabetic Rats

Implication for Diabetic NeuropathyS. Ishibashi1 , Natsuko Mori1 , Masako Shimada1 , T. Oka2 , H. Shimano1 , T. Gotoda1 , K. Komeda1 , S. Kawazu3 , T. Murase, Y. Yazaki1 , N. Yamada1
  • 1The Third Department of Internal Medicine
  • 2Department of Pathology, Faculty of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo
  • 3The Third Department of Internal Medicine, University of Gunma, Gunma, Japan
Further Information

Publication History

1992

1992

Publication Date:
14 March 2008 (online)

Summary

Apolipoprotein (apo) E secreted by macrophages plays an important role in nerve injury and repair. We investigated the disturbance of neural apo E metabolism in diabetic rats and its relation to diabetic neuropathy. In BB/W rats, genetically diabetes prone rats, the secretion of apo E from sciatic nerves was 3-fold greater than that in control rats. Furthermore, a similar enhancement of apo E secretion was observed in injured nerves of STZ-induced diabetic rats (2-fold) as compared with those of nondiabetic rats, and this was reversible with insulin treatment. Histological examination of the nerves revealed more extensive infiltration of mononuclear cells in the injured nerves of STZ-induced diabetic rats than in those of non-diabetic rats. This is consistent with the findings that chemotactic activities for mononuclear cells, which were released from injured nerves, were greater in the STZ-induced diabetic rats than in the non-diabetic rats. From these results we conclude that the recruitment of monocyte/mactophages into injured nerves is enhanced in diabetes, thereby causing derangement of neural apo E metabolism. These abnormalities might contribute to the development of diabetic neuropathy.

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