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Does irbesartan reduce chemerin expression in the renal tissues of streptozotocin-induced diabetic rats?
Does irbesartan reduce chemerin expression in the renal tissues of streptozotocin-induced diabetic rats?
Irbesartan reduces chemerin overexpression and RAS-related protein levels in the renal tissues of diabetic rats, suggesting a potential mechanism for its renoprotective effects.
Should not yet change practice in diabetic nephropathy; leaves open mechanistic translation of chemerin reduction to human CKD.
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.
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Yu et al. (2015) studied this question.
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