کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5507112 1536899 2017 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Macrophage ubiquitin-specific protease 2 modifies insulin sensitivity in obese mice
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Macrophage ubiquitin-specific protease 2 modifies insulin sensitivity in obese mice
چکیده انگلیسی


- USP2A controls macrophage population in mesenteric adipose tissue during obesity.
- Overexpression of USP2A in macrophages retards progression of insulin resistance.
- Overexpression of USP2A in macrophages represses high-fat diet-induced obesity.
- Macrophage USP2A controls insulin sensitivity of muscle dependent on adipocytes.

We previously reported that ubiquitin-specific protease (USP) 2 in macrophages down-regulates genes associated with metabolic diseases, suggesting a putative anti-diabetic role for USP2 in macrophages. In this study, we evaluate this role at both cellular and individual levels. Isolated macrophages forcibly expressing Usp2a, a longer splicing variant of USP2, failed to modulate the insulin sensitivity of 3T3-L1 adipocytes. Similarly, macrophage-selective overexpression of Usp2a in mice (Usp2a transgenic mice) had a negligible effect on insulin sensitivity relative to wild type littermates following a three-month high-fat diet. However, Usp2a transgenic mice exhibited fewer M1 macrophages in their mesenteric adipose tissue. Following a six-month high-fat diet, Usp2a transgenic mice exhibited a retarded progression of insulin resistance in their skeletal muscle and liver, and an improvement in insulin sensitivity at an individual level. Although conditioned media from Usp2a-overexpressing macrophages did not directly affect the insulin sensitivity of C2C12 myotubes compared to media from control macrophages, they did increase the insulin sensitivity of C2C12 cells after subsequent conditioning with 3T3-L1 cells. These results indicate that macrophage USP2A hampers obesity-elicited insulin resistance via an adipocyte-dependent mechanism.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemistry and Biophysics Reports - Volume 9, March 2017, Pages 322-329
نویسندگان
, , , , , , , , , , , , , ,