Mehrdad Ostadpoor,1,*Seyyed Hossein Heidari,2Pooria Rezaei,3Ahmad Zeinodini,4
1. Graduatedof Veterinary Medicine Faculty, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran 2. Graduatedof Veterinary Medicine Faculty, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran 3. Graduatedof Veterinary Medicine Faculty, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran 4. Graduatedof Veterinary Medicine Faculty, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
Introduction: The metabolic syndrome (MetS) also called insulin resistance syndrome was originally described in 1988. it refers to the commonly occurring disorder comprising central obesity, systemic hypertension, insulin resistance and atherogenic dyslipidemia. it is associated with accelerated atherosclerosis in response to chronic inflammation, vascular endothelial dysfunction and presents significantly increased cardiovascular risk. Scientists have outlined diagnostic criteria for metabolic syndrome, which designates values for obesity (waist circumference or BMI), triglyceride levels, HDL levels, hypertension, hyperglycemia and sometimes urine albumin or albumin : creatinine ratio. among the components of metabolic syndrome, the quantity of insulin resistance and abdominal obesity have increased during the last decade.
Methods: In the current study, key words including Sympathetic, Metabolic Syndrome and Risk Factor were reviewed from the list of Mesh and other credible websites including PubMed, Science Direct and Google Scholar over the past two decades and the data was organized.
Results: Result shows increasing sympathetic nerve activity is vital in the dissipation of energy following food consumption through activation of beta-receptors. it is proposed that chronic sympathetic nerve activity can potentiate gaining weight and leading to obesity as a consequence of diminished sensitivity of beta-adrenoceptors. also in vitro and vivo studies clearly show that prolonged adrenergic stimulation results in desensitization of beta-receptor mediated responses. down regulation of beta-adrenoceptors leading to a blunted thermogenic response to food can potentiate insulin resistance and perpetuate the negative feedback cycle between insulin governing sympathetic outflows. in support of a primary role of the sympathetic nervous system in metabolic abnormalities that cluster to form the MetS, several prospective studies clearly show that increasing noradrenaline levels can precede clinical symptoms of obesity and hypertension. another study shows the activation of sympathetic nerves in target organs like liver, pancreas, skeletal muscle, and adipose tissue can elicit acute catabolic responses. over activation of sympathetic nervous system is strongly associated with obesity and hypertension. in fact, enhanced Sympathetic nervous system activation exerts unfavorable effects like cardiac hypertrophy, arterial remodeling, and endothelial dysfunction on the cardiovascular system.
Conclusion: The sympathetic nervous system plays a pivotal role in regulating metabolic control. while acute sympathetic activation may be desirable under specific circumstances, it is clear that chronic stimulation of the sympathetic nervous system has the potential to augment risk for the MetS through the development of obesity, hyperglycaemia, insulin resistance, and hypertension.