New Perspectives on the Role of Hyperglycemia, Free Fatty Acid and Oxidative Stress in B-Cell Apoptosis

Message:
Abstract:
Apoptosis is a complex network of biochemical and molecular pathway with fine regulatory mechanisms that control the death event during several pathological situations in multi cellular organisms. It is the part of normal development that occurs in a variety of diseases and is known as aberrant apoptosis. Pancreatic β cell apoptosis is also a pathological feature which is common in both type 1 and type 2diabetes. There are several reasons through which apoptosis can be induced in β-cell. Metabolic abnormalities such as hyperlipidemia and hyperglycemia have been cited as critical mediator of cell death and may either trigger β-cell apoptosis. Persistent hyperglycemia causes increased production of free radicals that can damage initial β-cell in type I diabetes, impaired insulin production, release or function in type II diabetes. Also apoptosis plays an important role in several diabetic complications. The role of metabolic factors and their mechanism in β-cell apoptosis have been surveyed in this paper.
Language:
English
Published:
Iranian Journal of Diabetes and Obesity, Volume:6 Issue: 3, Autumn 2014
Pages:
142 to 147
magiran.com/p1411078  
دانلود و مطالعه متن این مقاله با یکی از روشهای زیر امکان پذیر است:
اشتراک شخصی
با عضویت و پرداخت آنلاین حق اشتراک یک‌ساله به مبلغ 1,390,000ريال می‌توانید 70 عنوان مطلب دانلود کنید!
اشتراک سازمانی
به کتابخانه دانشگاه یا محل کار خود پیشنهاد کنید تا اشتراک سازمانی این پایگاه را برای دسترسی نامحدود همه کاربران به متن مطالب تهیه نمایند!
توجه!
  • حق عضویت دریافتی صرف حمایت از نشریات عضو و نگهداری، تکمیل و توسعه مگیران می‌شود.
  • پرداخت حق اشتراک و دانلود مقالات اجازه بازنشر آن در سایر رسانه‌های چاپی و دیجیتال را به کاربر نمی‌دهد.
In order to view content subscription is required

Personal subscription
Subscribe magiran.com for 70 € euros via PayPal and download 70 articles during a year.
Organization subscription
Please contact us to subscribe your university or library for unlimited access!