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العنوان
Role of Soy Protein in Correcting Metabolic Disorders Induced in Rats Fed High Fructose Diet /
المؤلف
Ibrahim, Reham Abd El-Hamed Ahmed.
هيئة الاعداد
باحث / ريهام عبد الحميد احمد ابراهيم
مشرف / نهلة السيد العشماوى
مناقش / صفوت قاسم
مناقش / عاطف عبد الباقى
الموضوع
Pharmacy. Biochemistry.
تاريخ النشر
2020.
عدد الصفحات
126 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الصيدلة ، علم السموم والصيدلانيات (المتنوعة)
تاريخ الإجازة
12/1/2021
مكان الإجازة
جامعة طنطا - كلية الصيدلة - Biochemistry
الفهرس
Only 14 pages are availabe for public view

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from 161

Abstract

Fructose is a highly lipogenic, ketonic monosaccharide that is found in several fruits and is used as a sweetener in the food industry. Fructose consumption is associated with the dysregulation of adipokines and augmentation of proinflammatory processes. Additionally, there are many metabolic disorders induced by high fructose consumption due to the increased levels of FFA that activate the inhibitor kappa kinase β (IKK-β) and protein kinase C theta (PKCθ), which are related to the dysregulation of insulin signalling. Soy protein is a protein isolated from soybean. It is a rich source of dietary protein which provides the cells with essential amino acids and valuable macronutrients. The unique importance of soy protein could be attributed to that it contains isoflavones that are responsible for many biological and beneficial properties for maintenance of health. Isoflavones are known as phytoestrogens as they have estrogen-like effects which protect postmenopausal women from bone loss and maintain a healthy heart. Consumption of soy protein has been found to reduce serum concentrations of triglycerides. Soy protein also contributed to control of hyperglycemia, body weight, hyperlipidemia, and hyperinsulinemia. A novel NF-κB inhibitor, IMD-0354 (N-(3,5-bistrifluoromethylphenyl) – 5 - chloro -2-hydroxybenzamide), inhibits IKK-β and blocks IκB phosphorylation in the NF-κB pathway. The NF-κB signalling pathway plays an essential role in both inflammation and angiogenesis. The present work aimed to study the different metabolic disorders induced by chronic consumption of fructose. This work also aimed to evaluate the role and possible mechanism of action of soy protein in amelioration of inflammatory and metabolic disorders induced by over consumption of fructose in rat model. Seventy male Albino rats were divided into seven groups: normal control group, soy protein group, inhibitor (IMD) group (10 mg/kg IMD- 0354), HF group, HF-S group (HF + 20% soy protein isolate), HF-IMD (HF + 10 mg/kg IMD-0354), HF-S-IMD group (HF + 20% soy protein isolate +10 mg/kg IMD-0354). At the end of the experiment (8 weeks), rats were fasted overnight and weighed, then blood was withdrawn under anesthesia, fasting blood glucose was measured. Serum samples were separated for biochemical assay of insulin, and FFA. After blood collection, rats were sacrificed, then the liver samples were carefully excised and weighed. Samples of liver were used for histopathological examination, biochemical analysis of NF-kB, chrEBP, and PIR by ELISA. In the present study, rats fed on HF diet for 8 weeks developed signs of inflammation concomitant with some metabolic abnormalities including body weight gain, fat deposition in liver, hyperglycemia, hyperinsulinemia, IR, and dyslipidemia. These findings were supported by the histopathological changes in liver tissue of HF group, which showed periportal inflammatory cells infiltration associated with hepatic steatosis. Herein, treatment of rats with soy protein or IMD-0354 showed mild degree of hepatic vacuolation and mostly within normal limits. Moreover, HFS- IMD group was found to have normal degree of hepatic vacuolation nearly similar to that of normal control group. HF-S, HF-IMD, and HF-S-IMD groups showed a significant decrease in body weight gain, liver weight, and liver index compared to HF group. Serum levels of glucose, insulin, HOMA-IR and FFA were significantly reduced in HF-S, HF-IMD, and HF-S-IMD groups compared to HF group. Levels of chrEBP , and NFkB in liver tissue were significantly decreased in HF-S, HF-IMD, and HF-S-IMD groups compared to HF group. However, the level of PIR in liver tissue was significantly increased in HF-S, HF-IMD, and HF-S-IMD groups compared to HF group.