العلاقة بين مصل Nesfatin-1 و Adiponctin وتركيز Resistin والسمنة مع مرض السكري من النوع 2

محتوى المقالة الرئيسي

Baydaa Ahmed Abed
Layla Othman Farhan
https://orcid.org/0000-0002-5961-1338
Ashgan Slman Dawood

الملخص

 


            داء السكري الناجم عن مقاومة الأنسولين هو الدافع وراء السمنة. تم تحديد بين   نسفاتين -1 ، أديبونكتين  في العديد من الأعضاء ، بما في ذلك الجهاز العصبي المركزي وخلايا جزرالبنكرياس .  Nesfatin-1 ، له دور في دوائر التوازن التي تعمل على الطاقة الاستتبابية والتحكم في تناول الطعام. أديبونكتين هو بروتين شبيه بالكولاجين في البلازما تنتجه الخلايا الدهنية ويرتبط بتطور مقاومة الأنسولين (IR) ومرض السكري من النوع 2 (DMT2) وأمراض القلب والأوعية الدموية (CVD)   . تم تحديد Resisting لأول مرة على أنه هرمون خاص بالأنسجة الدهنية مرتبط بالسمنة ومرض السكري. كان الهدف من هذه الدراسة هو تقدير العلاقة بين   نسفاتين -1 ، أديبونكتين ، تركيز رسستين والسمنة مع DMT2 . أظهرت النتائج زيادة معنوية في مستوى نسفاتين 1 ومستوى الريسيستين في مجموعة مرضى السكري البدينين مقارنة بمجموعة السكري غير البدينين. اظهرت مستويات الأديبونكتين انخفاضًا معنويًا للغاية في مجموعة مرضى السمنة مقارنة بالمجموعة غير البدناء ومجموعة التحكم في السمنة.   نسفاتين 1 وبعض المتغيرات كانت له علاقة ارتباط موجبة مع (  BMI، insulin، HOMA-IR ) كما وجد ارتباط معنوي موجب لمصلي المقاومة مع  (BMI، WC، TG،  HOMA-IR  insulin ). بينما كان هناك ارتباط سلبي بين اديبونيكتين المصل مع (BMI, TG and HOMA-IR) . تشير نتائج الدراسة الحالية إلى أن nesfatin-1 قد يكون له دور في التحكم في تناول الطعام وكذلك تطوير مقاومة الانسولين في المرضى الذين يعانون من السمنة المفرطة.

تفاصيل المقالة

كيفية الاقتباس
1.
العلاقة بين مصل Nesfatin-1 و Adiponctin وتركيز Resistin والسمنة مع مرض السكري من النوع 2. Baghdad Sci.J [انترنت]. 1 يناير، 2024 [وثق 20 مايو، 2024];21(1):0117. موجود في: https://bsj.uobaghdad.edu.iq/index.php/BSJ/article/view/8119
القسم
article

كيفية الاقتباس

1.
العلاقة بين مصل Nesfatin-1 و Adiponctin وتركيز Resistin والسمنة مع مرض السكري من النوع 2. Baghdad Sci.J [انترنت]. 1 يناير، 2024 [وثق 20 مايو، 2024];21(1):0117. موجود في: https://bsj.uobaghdad.edu.iq/index.php/BSJ/article/view/8119

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