Daniela Jezova, M.D., Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia
It is well known that beta-adrenergic stimulation is a significant regulatory mechanism in the heart. Beta3 subtype of adrenergic receptors localized also in the human heart may protect the myocardium against adverse effects of excessive catecholamine stimulation. Stimulation of cardiac beta3-adrenoceptors may lead to a decrease in heart contractility. These receptors mediate lipolysis and thermogenesis in the adipose tissue. The action of catecholamines via beta-adrenoceptors is of particular importance under stress conditions. The sympathetic-adrenomedullary system is one of the two main stress systems. The stress-induced epinephrine and norepinephrine release depends on the type and intensity of the stress stimulus as well as on the actual state of the body. The aim of the present study was to test the hypothesis that stress associated with repeated immune challenge has an impact on beta3-adrenergic receptor gene expression in the adipose tissue and in the brain. Sprague-Dawley rats of both sexes were intraperitoneally treated either with vehicle or lipopolysaccharide (LPS) in increasing doses for 5 days (50-200 microg/kg). Two hours after the last injection, the retroperitoneal adipose tissue and selected brain regions were collected. Repeated LPS treatment was associated with body weight loss and increased anxiety-like behavior. LPS treatment decreased beta3-receptor gene expression in the white adipose tissue with higher values in males compared to females. In the adipose tissue, LPS administration reduced peroxisome proliferator-activated receptor gamma, leptin and adiponectin gene expression, but increased interleukin-6 expression, irrespective of sex. In LPS-treated animals of both sexes, beta3-receptor gene expression was increased in the prefrontal cortex but not the hippocampus. In conclusion, the changes in the gene expression of the regulatory factors in the adipose tissue are likely to contribute to the adaptive processes during stress of repeated immune challenge. Supported by APVV-14-0840.