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:: Volume 7, Issue 3 (Int J Mol Cell Med 2018) ::
Int J Mol Cell Med 2018, 7(3): 185-192 Back to browse issues page
Inhibition of Interleukin-1 Receptor-Associated Kinases 1/4, Increases Gene Expression and Serum Level of Adiponectin in Mouse Model of Insulin Resistance
Athena Rajaie1 , Mostafa Allahyari1 , Mahdieh Nazari-Robati1 , Hossein Fallah 2
1- Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
2- Department of Clinical Biochemistry, Afzalipour School of Medicine, Kerman University of Medical Sciences, Kerman, Iran. , hf59ma@gmail.com
Abstract:   (5317 Views)
Insulin resistance is a feature of most patients with type 2 diabetes mellitus. Epidemiological evidence suggests a correlation between inflammation and insulin resistant states such as obesity, but the underlying mechanisms are largely unknown. Interleukin-1 receptor-associated kinases (IRAK) play a central role in inflammatory responses by regulating the expression of various inflammatory genes in immune cells. This study was aimed to investigate the effect of IRAK inhibitor on gene transcription and serum concentration of adiponectin in insulin-resistant mice. Experimental mice were randomly divided into 6 groups: the healthy control group was fed a regular chow diet while other groups were fed with a high-fat diet for 12 weeks. After this period, animals were treated with IRAK inhibitor, pioglitazone, both IRAK and pioglitazone, and DMSO, for two weeks. Adiponectin gene expression level was analyzed by real-time PCR. Additionally, serum adiponectin levels were measured by ELISA. Homeostasis model assessment-adiponectin (HOMA-AD) as an insulin sensitivity index was calculated. IRAK inhibitor and pioglitazone increased significantly the expression of adiponectin gene. Also, adiponectin concentration in the control group (9.67±1.1 μg/ml) increased to 25.34±2.04 μg/ml in pioglitazone treatment group. IRAK inhibitor also increased adiponectin concentration (18.24±1.53 μg/ml) but did not show a synergistic effect with pioglitazone when administered simultaneously (26.66±2.5 μg/ml).  HOMA-AD was 0.33±0.04 in the pioglitazone-treated group, 0.6±0.13 in IRAK inhibitor group, and 0.31±0.03 in animals that received IRAKi and pioglitazone.  Our findings suggest that increased adiponectin secretion from adipose tissue mediated by IRAK inhibitor may increase the insulin sensitivity in an animal model of insulin resistance.
Keywords: Insulin resistance, Inflammation, Adiponectin, IRAK inhibitor
Full-Text [PDF 466 kb]   (1665 Downloads)    
Type of Study: Original Article | Subject: Clinical Biochemistry
Received: 2018/08/17 | Accepted: 2018/10/8 | Published: 2018/10/14
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Rajaie A, Allahyari M, Nazari-Robati M, Fallah H. Inhibition of Interleukin-1 Receptor-Associated Kinases 1/4, Increases Gene Expression and Serum Level of Adiponectin in Mouse Model of Insulin Resistance. Int J Mol Cell Med 2018; 7 (3) :185-192
URL: http://ijmcmed.org/article-1-922-en.html


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Volume 7, Issue 3 (Int J Mol Cell Med 2018) Back to browse issues page
International Journal of Molecular and Cellular Medicine (IJMCM) International Journal of Molecular and Cellular Medicine (IJMCM)
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