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10.1186/s12986-015-0016-3 http://scihub22266oqcxt.onion/10.1186/s12986-015-0016-3 C4462080!4462080!26064180     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nutr+Metab+(Lond) 2015 ; 12 (ä): ä Nephropedia Template TP {{tp|p=26064180|t=2015. Inflamed macrophage microvesicles induce insulin resistance in human adipocytes |pdf=|usr=}}{{26064180}} gab.com Text Inflamed macrophage microvesicles induce insulin resistance in human adipocytes JO: Nutr Metab (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=26064180 #FOAvip Background: Cytokines secreted by adipose tissue macrophages (ATMs) significantly alter adipocyte function, inducing inflammatory responses and decreasing insulin sensitivity. However, little relevant information is available regarding the role of microvesicles (MVs) derived from ATMs in macrophage-adipocyte crosstalk. Methods: MVs were generated by stimulation of M1 or M2 phenotype THP-1 macrophages and incubated with human primary mature adipocytes and differentiated adipocytes. Subsequently, insulin-stimulated phosphorylation of Akt (pAkt) and glucose uptake were determined. Glucose transporter 4 (GLUT4) translocation and nuclear translocation of nuclear factor (NF)-kappa B were also analyzed in treated adipocytes. Results: M1 macrophage-derived MVs (M1 MVs) significantly reduced protein abundance of insulin-induced Akt phosphorylation in human primary mature adipocytes and differentiated adipocytes, when compared with the same concentration of M2 macrophage-derived MVs (M2 MVs). In contrast to M2 MVs, which enhanced the insulin-induced glucose uptake measured by 2-NBDG, M1 MVs decreased this effect in treated adipocytes. M1 MVs treatment also brought about a significant increase in the nuclear translocation of nuclear factor (NF)-kappa B, coupled with a decrease in pAkt level and GLUT4 translocation compared with M2 MVs-treated adipocytes. These effects were reversed by BAY 11?7085, a NF- kappa B specific inhibitor. Conclusions: MVs derived from proinflammatory (M1) macrophages may, at least in part, contribute to the pathogenesis of obesity-induced insulin resistance, reducing insulin signal transduction and decreasing glucose uptake in human adipocytes, through NF-kappa B activation. Therefore, these MVs may be potential therapy candidates for the management of type 2 diabetes mellitus. Electronic supplementary material: The online version of this article (doi:10.1186/s12986-015-0016-3) contains supplementary material, which is available to authorized users. Twit Text FOAVip Inflamed macrophage microvesicles induce insulin resistance in human adipocytes ????Nutr Metab (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=26064180 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26064180 #FOAvip English Wikipedia <ref>{{Cite pmid|26064180}}</ref> Inflamed macrophage microvesicles induce insulin resistance in human adipocytes #MMPMID26064180 Zhang Y; Shi L; Mei H; Zhang J; Zhu Y; Han X; Zhu D Nutr Metab (Lond) 2015[]; 12 (ä): ä PMID26064180show ga Background: Cytokines secreted by adipose tissue macrophages (ATMs) significantly alter adipocyte function, inducing inflammatory responses and decreasing insulin sensitivity. However, little relevant information is available regarding the role of microvesicles (MVs) derived from ATMs in macrophage-adipocyte crosstalk. Methods: MVs were generated by stimulation of M1 or M2 phenotype THP-1 macrophages and incubated with human primary mature adipocytes and differentiated adipocytes. Subsequently, insulin-stimulated phosphorylation of Akt (pAkt) and glucose uptake were determined. Glucose transporter 4 (GLUT4) translocation and nuclear translocation of nuclear factor (NF)-kappa B were also analyzed in treated adipocytes. Results: M1 macrophage-derived MVs (M1 MVs) significantly reduced protein abundance of insulin-induced Akt phosphorylation in human primary mature adipocytes and differentiated adipocytes, when compared with the same concentration of M2 macrophage-derived MVs (M2 MVs). In contrast to M2 MVs, which enhanced the insulin-induced glucose uptake measured by 2-NBDG, M1 MVs decreased this effect in treated adipocytes. M1 MVs treatment also brought about a significant increase in the nuclear translocation of nuclear factor (NF)-kappa B, coupled with a decrease in pAkt level and GLUT4 translocation compared with M2 MVs-treated adipocytes. These effects were reversed by BAY 11?7085, a NF- kappa B specific inhibitor. Conclusions: MVs derived from proinflammatory (M1) macrophages may, at least in part, contribute to the pathogenesis of obesity-induced insulin resistance, reducing insulin signal transduction and decreasing glucose uptake in human adipocytes, through NF-kappa B activation. Therefore, these MVs may be potential therapy candidates for the management of type 2 diabetes mellitus. Electronic supplementary material: The online version of this article (doi:10.1186/s12986-015-0016-3) contains supplementary material, which is available to authorized users. äInflamed macrophage microvesicles induce insulin resistance in human a(epmc).pdf DeepDyve Pubget Overpricing