| First Author | Thatcher SE | Year | 2012 |
| Journal | Int J Hypertens | Volume | 2012 |
| Pages | 762094 | PubMed ID | 22518292 |
| Mgi Jnum | J:286373 | Mgi Id | MGI:6403603 |
| Doi | 10.1155/2012/762094 | Citation | Thatcher SE, et al. (2012) Deficiency of ACE2 in Bone-Marrow-Derived Cells Increases Expression of TNF-alpha in Adipose Stromal Cells and Augments Glucose Intolerance in Obese C57BL/6 Mice. Int J Hypertens 2012:762094 |
| abstractText | 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-alpha 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 marrow cells promotes inflammation in adipose tissue and augments obesity-induced glucose intolerance. |
