RETRACTED: Hypoadiponectinemia is caused by chronic blockade of nitric oxide synthesis in rats (Retracted article. See vol. 60, pg. 1355, 2011)

被引:29
作者
Hattori, S [1 ]
Hattori, Y [1 ]
Kasai, K [1 ]
机构
[1] Dokkyo Univ, Sch Med, Dept Endocrinol & Metab, Mibu, Tochigi 3210293, Japan
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2005年 / 54卷 / 04期
关键词
D O I
10.1016/j.metabol.2004.10.017
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Adiponectin is an adipocyte-derived anti-atherogenic protein. Adiponectin levels are decreased in patients and animal models with obesity, diabetes, and coronary artery disease. However, the mechanism by which adiponectin levels are reduced remains unknown. Since hypoadiponectinemia is closely linked to endothelial dysfunction, we examined the regulation of adiponectin in a rat model of chronic blockade of nitric oxide (NO) synthesis by N-omega-nitro-L-arginine methyl ester (L-NAME). Decreased production of NO and increased production of O-2(-) were observed in aorta from L-NAME-treated rats. Plasma adiponectin levels and adiponectin mRNA levels of adipose tissue were markedly decreased in L-NAME-treated rats. Cotreatment of pioglitazone (PIO) or allopurinol (ALL) with L-NAME restored plasma adiponectin concentration and fat adiponectin mRNA levels to control levels. Thus, adiponectin levels were decreased in L-NAME-treated rats, however, they returned to normal following administration of PIO due to transcriptional activation of the adiponectin gene, as well as administration of ALL, likely due to elimination of oxidative stress. Oxidative stress appears to be an important cause of hypoadiponectinemia. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:482 / 487
页数:6
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