Critical role of chemokine (C-C motif) receptor 2 (CCR2) in the KKAy + Apoe -/- mouse model of the metabolic syndrome.
Critical role of chemokine (C-C motif) receptor 2 (CCR2) in the KKAy + Apoe -/- mouse model of the metabolic syndrome.
复制标题
趋化因子（C-C基序）受体2（CCR2）在代谢综合征的KKAY + APOE - / - 小鼠模型中的关键作用。
DOI：
10.1007/s00125-011-2248-8
复制
发表时间：
2011-10
期刊：
影响因子：
8.2
通讯作者：
Ahuja, S. S.
中科院分区：
文献类型：
--
作者：
Martinez, H. G.;Quinones, M. P.;Jimenez, F.;Estrada, C. A.;Clark, K.;Muscogiuri, G.;Sorice, G.;Musi, N.;Reddick, R. L.;Ahuja, S. S.
关键词：
Chemokines and their receptors such as CCR2 may contribute to the pathogenesis of metabolic syndrome (MetS) via their effects on inflammatory monocytes (IMo). It is thought that increased CCR2-driven IMo accumulation in the epididymal fat pads, favors the development of insulin resistance. Ultimately, resulting hyperglycemia and dyslipidemia contribute to the development of MetS complications such as cardiovascular disease (CVD) and diabetic nephropathy (DN). Our goal is to elucidate the role of CCR2 and IMo in a model that resembles human MetS. We generated a model of MetS by backcrossing KKAy+ with Apoe−/− mice (KKAy+Apoe−/−) and w studied the role of CCR2 in this model system. KKAy+Apoe−/− mice were characterized by the presence of obesity, insulin resistance, dyslipidemia and increased systemic inflammation. Additionally, in this model we described two MetS complications: atherosclerosis and DN. Also, we show that genetic inactivation of CCR2 in KKAy+Apoe−/− mice protects against MetS as well as atherosclerosis and DN. This protective phenotype was associated with reduced number of IMo in the liver and muscle but not the epididymal fat pads or circulating levels of adipokines such as leptin, resistin and adiponectin. Interestingly, the proportion of IMo in the liver, pancreas and muscle but not the epididymal fat pads correlated significantly with peripheral glucose levels. CCR2-driven IMo accumulation in the liver and muscle may be a critical pathogenic factor in the development of MetS.
登录
查看更多内容
影响因子：
16.2
作者：
Ford, ES
通讯作者：
Ford, ES
影响因子：
2.8
作者：
Haffner, SM
通讯作者：
Haffner, SM
影响因子：
5.3
作者：
Kuziel, WA;Dawson, TC;Maeda, N
通讯作者：
Maeda, N
DOI：
10.1152/ajprenal.1995.268.1.f82
发表时间：
1995-01-01
期刊：
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY
影响因子：
--
作者：
PAGTALUNAN, ME;RASCH, R;MEYER, TW
通讯作者：
MEYER, TW
影响因子：
8.3
作者：
Ohashi, Koji;Kihara, Shinji;Shimomura, Iichiro
通讯作者：
Shimomura, Iichiro