Consumption of a high-galactose diet induces diabetic-like changes in the inner ear.

Published

Journal Article

Diabetes mellitus is a disease that affects multiple organ systems. In our laboratory it has been shown that there is a significant loss of outer hair cells in genetically diabetic rats. Galactosemia can also produce diabetic-like changes. This study was performed to demonstrate whether these changes also occur in the cochlea. Three groups of Sprague-Dawley rats were used and fed either a control diet, a 50% galactose diet, or a 50% galactose diet with the addition of an aldose reductase inhibitor. After 6 months the animals were killed, and the cochleas were removed, fixed, and stained. Diabetes-induced damage was assessed by counting the hair cells and calculating the neuroganglion cell density. The histopathologic changes induced by galactose were manifested as outer hair cell loss and a decrease in neuroganglion cell density. Control animals had the least amount of hair cell loss and the greatest neuroganglion cell density of all three groups. Galactose-only animals demonstrated the most pronounced changes in both hair cell loss and neuroganglion cell degeneration; however, only changes of neuroganglion cell density in the basal turn were significant. The addition of an aldose reductase inhibitor provided inconclusive results in both hair cell determination and neuroganglion cell density; however, generally the inhibitor partially prevented the damage produced by galactose. These results suggest that a high-galactose diet can induce diabetic-like changes in the cochlea.

Full Text

Duke Authors

Cited Authors

  • Raynor, E; Robison, WG; Garrett, CG; McGuirt, WT; Pillsbury, HC; Prazma, J

Published Date

  • December 1995

Published In

Volume / Issue

  • 113 / 6

Start / End Page

  • 748 - 754

PubMed ID

  • 7501387

Pubmed Central ID

  • 7501387

Electronic International Standard Serial Number (EISSN)

  • 1097-6817

International Standard Serial Number (ISSN)

  • 0194-5998

Digital Object Identifier (DOI)

  • 10.1016/s0194-59989570015-3

Language

  • eng