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E. M. Rocha, A. C. Dias, C. M. Modulo, A. G. Jorge, R. Bertazolli Filho; Influence of Insulin Treatment on Lacrimal Gland and Ocular Surface of Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2008;49(13):124.
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© ARVO (1962-2015); The Authors (2016-present)
Previous studies have observed structural, functional and molecular alterations in the lacrimal gland (LG) and ocular surface (OS) of rodents and humans with chronic diabetes mellitus. The aim of this study was a) to compare the expression of markers of oxidative stress and histological markers of disease and b) to evaluate whether insulin treatment inhibits LG and OS alterations.
Diabetes was induced in male Wistar rats with a single intravenous injection of streptozotocin and a subgroup was treated with insulin. After 5 and 10 weeks, LG and OS of the three groups (n=5-10/group) were compared and analyzed for the expression of malonaldehyde (MDA) and peroxidase. Impression cytology (IC) was used to compare the ocular surface epithelia and the Schirmer test was sued to evaluate tear secretion.
After 10 weeks, no significant difference was found in OS epithelial morphology (IC). After 5 weeks, changes in LG morphology and increased numbers of lipofucsin-like inclusions were observed in diabetic but not insulin-treated rats. After 10 weeks, MDA levels were significantly higher in diabetic rats, but similar to control in insulin-treated diabetic rats (P= 0.03, P= 0.02). After 5 weeks, peroxidase levels were higher in diabetic rats, returning to levels similar to control after 10 weeks (P=0.02 and 0.096, respectively).
Our data indicates that diabetes induces histological alterations in LG and that hyperglycemia-related oxidative stress may participate in diabetic dry eye syndrome. The effect of insulin replacement suggests direct hormone action and/or benefit by mild metabolic control.
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