deficiency of ace2 in bone-marrow-derived cells increases expression of tnf-α in adipose stromal cells and augments glucose intolerance in obese c57bl6 mice缺乏ace2在从骨髓细胞增加tnf-α在脂肪基质细胞的表达和增强肥胖c57bl6小鼠的葡萄糖耐受不良.pdfVIP

Hindawi Publishing Corporation International Journal of Hypertension Volume 2012, Article ID 762094, 8 pages doi:10.1155/2012/762094 Research Article Deficiency of ACE2 in Bone-Marrow-Derived Cells Increases Expression of TNF-α in Adipose Stromal Cells and Augments Glucose Intolerance in Obese C57BL/6 Mice Sean E. Thatcher, Manisha Gupte, Nicholas Hatch, and Lisa A. Cassis Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY 40536-0200, USA Correspondence should be addressed to Lisa A. Cassis, lcassis@ Received 1 September 2011; Revised 17 October 2011; Accepted 24 October 2011 Academic Editor: Robson Santos Copyright © 2012 Sean E. Thatcher et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Deficiency of ACE2 in macrophages has been suggested to promote the development of an inflammatory M1 macrophage phenotype. We evaluated effects of ACE2 deficiency in bone-marrow-derived stem cells on adipose inflammation and glucose tolerance in C57BL/6 mice fed a high fat (HF) diet. ACE2 activity was increased in the stromal vascular fraction (SVF) isolated from visceral, but not subcutaneous adipose tissue of HF-fed mice. Deficiency of ACE2 in bone marrow cells significantly increased mRNA abundance of F4/80 and TNF-α in the SVF isolated from visceral adipose tissue of HF-fed chimeric mice, supporting increased presence of inflammatory macrophages in adipose tissue. Moreover, deficiency of ACE2 in bone marrow cells modestly augmented glucose intolerance in HF-fed chimeric mice and increased blood levels of glycosylated hemoglobin. In summary, ACE2 deficiency in bone ma