کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2040482 1073113 2014 14 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis
ترجمه فارسی عنوان
گیرنده 4 مانند سلول ایمنی مانند سلول های بنیادی فیبروز بافت چربی و وابسته به آنزیم آندوتوکسمی
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم کشاورزی و بیولوژیک (عمومی)
چکیده انگلیسی


• Adipose tissue fibrosis is associated with obesity-induced insulin resistance
• Macrophage Toll-like receptor 4 (TLR4) is required for adipose tissue fibrosis
• TLR4 ligand, lipopolysaccharide, induces fibrosis through the profibrotic factor TGFβ1
• Obesity and endotoxemia promote fibrosis through adipose tissue immune cell TLR4

SummaryAdipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibrosis. Continuous low-dose infusion of the Toll-like receptor 4 ligand, lipopolysaccharide, promotes adipose tissue fibrosis. Ex vivo, lipopolysaccharide-mediated induction of fibrosis is prevented by antibodies against the profibrotic factor TGFβ1. Together, these results indicate that obesity and endotoxemia favor the development of adipose tissue fibrosis, a condition associated with insulin resistance, through immune cell Toll-like receptor 4.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 7, Issue 4, 22 May 2014, Pages 1116–1129
نویسندگان
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