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Sorbitol Accumulation In Ascorbic Acid Treated Schwann Cells Cultured In High Glucose Medium
Author(s) -
Suzuki T,
Yashima S,
Taniko K,
Mizuno K,
Suzuki T,
YabeNishimura C.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000.005003183.x
Subject(s) - sorbitol , basement membrane , ascorbic acid , schwann cell , aldose reductase , aldose reductase inhibitor , chemistry , glomerular basement membrane , medicine , endocrinology , axon , extracellular matrix , microbiology and biotechnology , biochemistry , biology , enzyme , kidney , food science , glomerulonephritis
Unless the expression of aldose reductase (AR) was upregulated, sorbitol was not accumulated under high glucose conditions in Schwann cells isolated from adult rat sciatic nerves (1). In the peripheral nerve, however, Schwann cells of both myelinated and un‐myelinated fibers are ensheathed by the basement membrane. To evaluate the effect of basement membrane formation on sorbitol accumulation, we examined the sorbitol levels in Schwann cells pre‐cultured for 12 days in the medium containing 50μg/ml ascorbic acid and 20nM progesterone that elicit basement membrane synthesis on the plate coated with extracellular matrix. In the cells cultured in ascorbic acid containing medium, type IV collagen, one of the basement membrane components, was detected. When these cells were incubated with 50mM glucose for 6 days, a significant level of sorbitol accumulation was observed without any change in the activity of AR and SDH. Fidarestat, an inhibitor of AR, decreased the sorbitol levels in a dose‐dependent manner. Increased fructose levels in these cells were simultaneously suppressed by the addition of fidarestat. Our findings therefore suggest that accumulation of sorbitol in Schwann cells takes place under diabetic conditions, only when cells are ensheathed by the basement membrane. (1) Suzuki, T., et al. (1999). J. Neurosci. Res., 57, 495‐503.