کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2195623 1550854 2016 15 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Endoplasmic reticulum stress regulates inflammation and insulin resistance in skeletal muscle from pregnant women
ترجمه فارسی عنوان
استرس رتیکولوم اندوپلاسمی تنظیم التهاب و مقاومت به انسولین در عضلات اسکلتی را از زنان باردار
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
چکیده انگلیسی


• ER stress is increased in skeletal muscle with GDM and obese pregnant women.
• Suppression of ER stress decreased inflammation in skeletal muscle.
• Suppression of ER stress improved insulin resistance in skeletal muscle.

Sterile inflammation and infection are key mediators of inflammation and peripheral insulin resistance associated with gestational diabetes mellitus (GDM). Studies have shown endoplasmic reticulum (ER) stress to induce inflammation and insulin resistance associated with obesity and type 2 diabetes, however is paucity of studies investigating the effects of ER stress in skeletal muscle on inflammation and insulin resistance associated with GDM. ER stress proteins IRE1α, GRP78 and XBP-1s were upregulated in skeletal muscle of obese pregnant women, whereas IRE1α was increased in GDM women. Suppression of ER stress, using ER stress inhibitor tauroursodeoxycholic acid (TUDCA) or siRNA knockdown of IRE1α and GRP78, significantly downregulated LPS-, poly(I:C)- or IL-1β-induced production of IL-6, IL-8, IL-1β and MCP-1. Furthermore, LPS-, poly(I:C)- or TNF-α-induced insulin resistance was improved following suppression of ER stress, by increasing insulin-stimulated phosphorylation of IR-β, IRS-1, GLUT-4 expression and glucose uptake. In summary, our inducible obesity and GDM-like models suggests that the development of GDM may be involved in activating ER stress-induced inflammation and insulin resistance in human skeletal muscle.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 425, 15 April 2016, Pages 11–25
نویسندگان
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