PurposeThe purpose of the study was to assess potential interactions of light exposure and hyperglycemia upon ocular complications in diabetic rats.MethodsStreptozotocin-induced (STZ-induced) diabetic rats (N = 39) and non-diabetic rats (N = 9) were distributed into eight groups according to the irradiance and color of the light phase during the 12/12-hour light/dark regime. Follow-up lasted 90 days and included assessment of cataract development and electroretinogram (ERG) recordings. Stress to the retina was also assessed by glial fibrillary acidic protein immunocytochemistry.ResultsCataract development was fast in diabetic rats that were exposed to unattenuated white light or to bright colored lights during the light phase. Diabetic rats that were kept under attenuated brown or yellow light during the light phase exhibited slower rate of cataract development. Electroretinogram responses indicated very severe retinal damage in diabetic rats kept under bright colored lights in the blue-yellow range or bright white light during the light phase. Electroretinogram damage was milder in rats kept under bright red light or attenuated yellow or brown light during the light phase. Glial fibrillary acidic protein expression in retinal Müller cells was consistent with ERG assessment of retinal damage.ConclusionsAttenuating white light and filtering out short wavelengths have a protective effect on the eyes of diabetic rats as evident by slower rate of cataract formation and a smaller degree of retinal damage.Translational RelevanceOur findings suggest that special glasses attenuating light exposure and filtering out short wavelengths (400–530 nm) may be beneficial for diabetic patients.
Objectives. Diabetes mellitus is an endemic disease of the current era. It is important to treat it properly. All antidiabetic medications have side effects and various safety profiles.Case report. Fifty-two years old patient with type II diabetes mellitus, who had spontaneous cutaneous and intra muscular bleeding after starting treatment with Exenatide. The patient’s history did not include any kind of spontaneous bleeding. Investigations did not reveal abnormal platelets count and function or coagulation profile. The use of the Exenatide was discontinued and during one year of follow-up, the patient did not experience an additional occurrence of spontaneous bleeding.Conclusions. To the best of our knowledge, this is the first report of spontaneous bleeding probably caused by Exenatide. The exact pathophysiology, by which the drug can cause spontaneous bleeding, is still not clear and has to be revealed.
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