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العنوان
Effect of vitamin D3 on diabetic nephropathy and neuropathy in rats /
المؤلف
Brayek, Huda Ibrahim Abd El Hafiz.
هيئة الاعداد
باحث / هذى ابراهيم عبذ الحفيظ بريك
مشرف / عادل حسين عمر
مشرف / عبد الرحمن عبد الفتاح ياسين
مشرف / ماجدة احمد منصور
الموضوع
Pharmacology. vitamin D3. diabetic nephropathy. diabetic neuropathy.
تاريخ النشر
2015.
عدد الصفحات
195 p. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/12/2015
مكان الإجازة
جامعة المنوفية - كلية الطب - الفارماكولوجيا الاكلينيكية
الفهرس
Only 14 pages are availabe for public view

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Abstract

y morbidity and mortality worldwide. Diabetic nephropathy is a common cause of end stage of renal disease. Diabetic nephropathy is a progressive and irreversible renal disease characterized by the accumulation of extracellular matrix in glomerular basement membrane (glomerulosclerosis) and kidney interstitial tissue that eventually leads to renal failure. Diabetic peripheral neuropathy is the most common complication of long-standing diabetes mellitus, which frequently results in clinically significant morbidities as pain, foot ulcers and amputation. Vitamin D3 (calcitriol) is an activate metabolite of vitamin D in the body, in addition to its classical role in calcium and bone homeostasis, vitamin D3 has been discovered to have many other roles such as immunoregulation, blood pressure control, antineoplastic effect and β -cell regulation through its binding to VDRs, which discovered in many tissues including β-cells of pancreas, kidney cells and peripheral nervous system. Many cellular, preclinical and observational studies suggest a role for vitamin D deficiency in the pathogenesis of both T1DM and T2DM. The present study is designed to investigate the effect of vitamin D3 on diabetic nephropathy and neuropathy of streptozotocin induced type 2 diabetes in rats. Forty male Sprague- Dawley rats are fed with high-fat and high-sugar diet (feed formula: 67% normal diet , 20% sucrose , 10% tried lard , 2% cholesterol , 1% bile salts) and water for 6 weeks. Then, rats are injected IP with a single dose of freshly dissolved STZ (30 mg/kg
body weight) in a pH 4.5 citric acid buffer after an overnight fasting. On the seventh day after the injection of STZ, rats with FBG ≥126 mg/dl and/or 2hBG ≥ 200 mg/dl were considered diabetic and used in the experiment. Rats were classified into 5 groups, 8 rats for each group: 1- Normal control group 1 (G-1): Received a single dose of citrate buffer IP (vehicle for STZ) and coconut oil orally by gavage (vehicle of vitamin D3) for 4 weeks. 2- Diabetic untreated group 2 (G-2): Received, by oral gavage, coconut oil for 4 weeks. 3- Diabetic treated with insulin group 3 (G-3): Received SC injection of (10U/kg body weight) NPH insulin daily during the entire period of the experiment (4 weeks) and last injection was given 24 h before sacrificing the rats. 4- Diabetic treated with calcitriol group 4 (G-4): Received calcitriol daily by oral gavage in a dose of 0.03μg/kg body weight for 4 weeks. 5- Diabetic treated with insulin and calcitriol group 5 (G-5): Received both insulin and calcitriol as group 3 and group 4 respectively for 4 weeks.