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العنوان
Possible Role of L-Carnitine in Improvement of Hepatic and Metabolic Changes in Hyperuricemic and Hyperuricemic- Fructose Supplemented Rats/
المؤلف
ElKady,Amr Hisham .
هيئة الاعداد
باحث / عمرو هشام القاضي
مشرف / بطا محمد علي الكفوري
مشرف / منى أحمد أحمد
مشرف / نهى نوح لاشين
تاريخ النشر
2017.
عدد الصفحات
247.p;
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/1/2017
مكان الإجازة
جامعة عين شمس - كلية الطب - Physiology
الفهرس
Only 14 pages are availabe for public view

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from 247

Abstract

Introduction: Uric acid, a purine metabolite, is generated by the action of the enzyme, xanthine oxidase (XO), which catalyzes the last two steps of uric acid formation: hypoxanthine to xanthine and from xanthine to uric acid.
Aim of the Work: This study is designed to throw more light on the role of fructose feeding in aggravation of the possible metabolic and hepatic effects of hyperuricemia, and to probe the ability of L- Carnitine in restoring the energy balance of the cell and hence its subsequent ability to manage the possible deleterious effects of hyperuricemia.
Materials and Methods: This study was carried out on 50 adult male albino rats, initially weighing 150-180 grams. Rats were purchased from Ophthalmic Diseases Research Institute, Giza, and were housed in the Physiology Department Animal House, Faculty of Medicine, Ain Shams University, under standard conditions of boarding at room temperature 22-25 oC, 12 hours light dark cycle and free access to food and water- ad libitum- throughout the whole period of the study. Rats were kept in plastic cages (4 rats /cage) for one week prior to experimental procedures for acclimatization. Regular meals were introduced daily at 8 a.m. Rats were fed standard rat diet (consisted of 400 ml milk, 600 gm balady bread and vegetables in each Kg).
Results: As shown in table (1) and figure (11), plasma uric acid level was significantly increased in untreated hyperuricemic rats (group II), untreated hyperuricemic fructose supplemented rats (group III), L-Carnitine treated hyperuricemic rats (group IV) and L- Carnitine treated hyperuricemic fructose supplemented rats (group V) compared to control rats (group I).
Conclusion: Hyperuricemia caused deleterious metabolic and hepatic effects. Artificial fructose supplementation, in the current study, aggravated the picture of hyperuricemia and showed more deleterious metabolic and hepatic effects.
Recommendations: The growing consumption of sweetened beverages containing fructose in developed and developing countries must be controlled and considered as important as the animal protein diet in the genesis of hyperuricemia.