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Ana C. Dias, Carolina M. Módulo, Leonardo T. Malki, Gabriela S. Ferrreira de Castro, Jayter S. de Paula, Eduardo M. Rocha, Monica Alves; Insulin Prevents Change in the Mechanism of Secretion in Lacrimal Gland of Diabetic Rats. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3744.
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In lacrimal glands (LG), cholinergic agonists transmit signals that regulate release of secretory products and those events are governed in cytoplasm by groups of proteins known as rab and SNARE. The aim of the present work was to compare the expression of the secretory apparatus in lacrimal glands of diabetic and control rats.
Diabetes was induced in male Wistar rats with a single intravenous streptozotocin or vehicle and a sub group was than treated every other day with insulin. After 10 weeks, LG of the three groups (n=5/group) had the structure compared, and analyzed for expression of acetylcholine (Ach). Western blot and RT-PCR was used to compare the expression of rab and SNARE secretory factors. Structure of acinar cells were observed by Transmission Eletronic Mycroscopy (TEM).
After 10 weeks of diabetes, it was not observed significantly differences in the Ach levels among the three groups. The mRNA expression of Rab3D, Rab 27b and VAMP2 were not changed by diabetes or insulin treatment. Western blot analysis had shown that Rab 27b, syntaxin and VAMP2 proteins were significantly reduced in LG of DM compared to controls (P<0.05). Insulin treatment increases the expression of Rab 27b and syntaxin to the control levels while Vamp 2 reduction was not reverted by insulin. Enlarged vesicles and reduced number of dark vesicles were observed in LG of diabetic group at EM, and they were in part preserved in the insulin treated group.
The significant alterations in LG structure and function in DM also includes reduction in proteins of the exocytosis machinery revealing a pos-transcriptional effect of the disease in diabetic LG. Those events were, in part, reverted by insulin replacement, which may be directly driven to acinar cells or secondary to glycemia control.
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