AI Article Synopsis
- The congenic SHR/N-cp rat serves as a model for studying non-insulin-dependent diabetes, with previous findings highlighting significant outer hair cell (OHC) loss in diabetic rats at younger ages.
- In this study, researchers compared the inner ear health of 10.5-month-old diabetic rats with euglycemic controls while also looking at differences between obese and lean phenotypes, as well as dietary carbohydrate sources.
- Results showed consistent OHC loss in diabetic rats, with more damage observed in sucrose-fed diabetics compared to starch-fed ones, indicating a link between diabetes and inner ear damage, influenced by blood sugar levels and genetic factors.
Article Abstract
The congenic spontaneous hypertensive/National Institutes of Health (Bethesda, Md)-corpulent rat (SHR/N-cp) is a model for non-insulin-dependent diabetes mellitus. A previous study in our laboratory found significant loss of outer hair cells (OHC) in diabetic rats at 5.0 months of age. Our present study was designed to further evaluate the effects of the diabetic state on the inner ear in 10.5-month-old rats. The following comparisons were made: diabetic vs euglycemic control animals; obese vs lean phenotypes; and sucrose vs starch as the source of dietary carbohydrate. Cochleas were removed, fixed, stained, mounted on slides, and analyzed for OHC loss. We found a significant OHC loss in the cochleas of all diabetic animals. No statistical difference was found when comparing obese and lean phenotypes. Increased OHC loss was observed in all sucrose-fed vs starch-fed diabetic animals, although this increase was not statistically significant. Compared with an earlier study, an increase in OHC loss was also noted in the 10.5-month-old lean SHR/N-cp animals. Our results indicate that there is a relationship between non-insulin-dependent diabetes mellitus and inner ear damage and suggest that OHC loss is related to hyperglycemia and a genetic predisposition for glucose intolerance.
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| http://dx.doi.org/10.1001/archotol.1992.01880040059010 | DOI Listing |
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