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العنوان
The correlation between serum omentin-1 levels and insulin resistance in type 2 diabetic women /
الناشر
Sherry Elisha Fayez ,
المؤلف
Sherry Elisha Fayez
هيئة الاعداد
باحث / Sherry Elisha Fayez
مشرف / Nehal Hamdy Elsaid
مشرف / Noha Adly Sadik
مشرف / Nagwa Abdelghaffar Mohammed
تاريخ النشر
2016
عدد الصفحات
149 P. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب الباطني
تاريخ الإجازة
11/5/2016
مكان الإجازة
جامعة القاهرة - كلية الطب - Internal Medicine
الفهرس
Only 14 pages are availabe for public view

from 180

from 180

Abstract

Adipose tissue has been shown to secrete a variety of bioactive peptides, called adipokines that can potentially impact on glucose and lipid metabolism (Despres et al., 2008). Recently, a new protein omentin (also named omentin-1, intelectin, intelectin- 1, endothelial lectin and intestinal lactoferrin receptor) has been identified as a major visceral (omental) fat secretory adipokine (Gursoy et al., 2010). These adipokines play important roles in carbohydrate and lipid metabolism, homeostasis, insulin resistance, diabetes, atherosclerosis, vascular endothelial dysfunction, inflammation, and cardiovascularfunction. (Zhong X et al.,2011). Omentin -1 is highly and selectively expressed in visceral adipose tissue relative to subcutaneous adipose tissue. (Shibata et al.,2012). Visceral obesity is reported more pathogenic than subcutaneous obesity in promoting insulin resistance, type 2 diabetes and cardiovascular disease. (Gualillo et al., 2007; Chung et al., 2009; Grundy, 2004). Insulin resistance should be conceptualized in a very broad manner that takes into account the interplay between nutrition, glucose, insulin and adipokines in various metabolic important tissues. (Hossein-nezhad et al.,2012). While omentin is highly expressed in human visceral fat tissue,circulating omentin levels are reduced in obese subjects . (De Souza{u2013}Batista et al., 2007). Omentin is also down-regulated in association with obesity- linked metabolic disorders including insulin resistance, glucose intolerance and type 2 diabetes. (De Souza{u2013}Batista et al., 2007; Tan et al., 2008; Pan et al., 2010)