Effect of Irbesartan on Chemerin in the Renal Tissues of Diabetic Rats

• Main Authors: Qiu-Xia Yu, Hong Zhang, Wen-Hui Xu, Fei Hao, Su-Lai Liu, Meng-Meng Bai, Jia-Wei Mu, Hui-Juan Zhang
• Format: Article
• Language: English
• Published: Karger Publishers 2015-09-01
• Series: Kidney & Blood Pressure Research
• Subjects: Renin-angiotensin system; Irbesartan; Chemerin; Diabetic nephropathy
• Online Access: http://www.karger.com/Article/FullText/368523
• ISSN: 1420-4096; 1423-0143

Background/Aims: Chemerin was introduced as a novel adipokine that plays a crucial role in insulin signaling and diabetic nephropathy. Serum chemerin levels are significantly elevated in type 2 diabetes patients with macroalbuminuria. However, the underlying mechanisms remain unclear. We conducted a preliminary investigation of the effects of the renin-angiotensin system (RAS) on chemerin expression in streptozotocin-induced diabetic rats. Methods: Streptozotocin-induced diabetic rats were randomized into control, diabetic, and irbesartan-treated groups. Real-time polymerase chain reaction was used to detect mRNA expression of chemerin, angiotensin II type 1a receptor (AT1a), angiotensin II type 1b receptor (AT1b) and angiotensin II type 2 receptor (AT2). Immunohistochemical staining was used to detect chemerin in renal tissues. Results: Expression levels of chemerin in renal tissues were significantly elevated in the diabetic group compared to the control group. In the irbesartan-treated group, chemerin expression levels and RAS-related protein levels (i.e. AT1a and AT1b) were markedly decreased compared to the diabetic group. Irbesartan treatment reduced chemerin overexpression and RAS-related protein levels in diabetic rats (i.e. AT1a and AT1b). Conclusion: Irbesartan may inhibit intrarenal RAS in diabetic rats, which may affect the expression of chemerin in the kidneys; however, the precise underlying mechanism remains to be determined.