:: Volume 5, Issue 4 (12-2003) ::
2003, 5(4): 227-235 Back to browse issues page
Effect of α2-adrenergic antagonist on some factors secreted by adipose tissue in obese male rats
F Esfandi , N Pajhan , T Komeili Movahed , N Mohamad Taghvaei
, amin1651@yahoo.com
Abstract:   (25149 Views)
Introduction: Obesity is a major risk factor for type 2 diabetes, hypertension, hyperlipidemia, cardiovascular disease and certain types of cancer. Furthermore, obesity is associated with insulin resistance and hyperinsulinaemia. Hormones and cytokines such as leptin and TNF- are produced by adipose tissue and have a key role in insulin resistance of obesity. The purpose of this study was to examine the effects of peripheral administration of yohimbine on some of adipose factors. Materials and Methods: Experiments were carried out on two groups of male rats: lean control group (fed standard purina rodent chow) and obese group (fed cafeteria diet). A blood sample was taken from each rat, after exposure to diet for 18 weeks. The obese group were randomly divided into two groups. Group I was injected with 4mg/kg yohimbine and group II received the equal volume of saline. Blood samples were taken 30, 60, and 120 min after drug or saline injection. Results: Insulin level was significantly increased 30 and 60 minutes after injection (P<0.05). TNF- and leptin levels were decreased (P<0.05) while FFA level was increased in response to yohimbine, 30 minutes after injection. Glucose level was increased but it was lower than control group during 120 minutes. Conclusion: It has been shown previously that cAMP is the main regulatory factor of leptin, TNF- and FFA in adipocytes. In comparison to the obtained results in the control group, we conclude that probably sensitivity of – adrenergic receptors and /-AR proportion are increased in obesity.
Keywords: Obesity, – adrenergic receptor, Yohimbine, cAMP, Leptin, TNF-, FFA
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Type of Study: Original | Subject: Endocrinology
Received: 2006/11/28 | Published: 2003/12/15


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Volume 5, Issue 4 (12-2003) Back to browse issues page