RRML - Chronic Stress, Neuroendocrine Disorders and Metabolic Syndrome

ISSN online: 2284-5623

ISSN-L: 1841-6624

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Concept, Design & Programming
Dr. Adrian Man

Nr. 19(3)/2011

Chronic Stress, Neuroendocrine Disorders and Metabolic Syndrome

Ioana Brudaşcă, Mircea Cucuianu


More than 50 years ago clinicians had suggested that frequent association of obesity with arterial hypertension and with atherosclerotic vascular disease should involve some common pathogenic mechanisms including certain neuroendocrine disorders – a hypothesis being now supported by experimental and by clinical case-control studies. Daily cortisol secretion measured in saliva had higher levels in subjects at high stress comparativeley to subjects at low stress. A case control study emphasized that when compared to controls, the subjects displaying features of the metabolic syndrome were also presenting higher urinary elimination of cortisol and catecholamines metabolites, as well as higher serum levels of interleukin - 6 and CRP. It was therefore concluded that autonomic, adrenocortical and inflammatory causes are involved in the development of metabolic syndrome, which can be a intermediate on the pathway between long term psychosocial stress and coronary artery disease. Visceral obesity may be a target of activated sympathoadrenal system, as adipose tissue of such patients is endowed with numerous highly sensitive β3 adrenoreceptors. Subsequent activation of hormone dependent lipase within this hypertrophic adipose tissue would trigger the release of fatty acids into the portal flow leading to hepatic steatosis and insulin resistance. Free fatty acids taken up into specific receptors would stimulate the synthesis of plasminogen activator inhibitor -1 (PAI-1). The interaction of free fatty acids derived from a high fat diet with a G protein-coupled transmembrane receptor (the GPR-40, preferentially expressed on pancreatic β cells) would mediate an excessively increased glucose stimulated insulin secretion, leading to hyperinsulinemia and metabolic syndrome. Beta –adrenergic stimulation would also activate the renin-angiotensin–aldosterone system within adipose tissue of obese patients. Visceral obesity and neuroendocrine disorders are also involved in the pathogenesis of renal disease and in the hyperinsulinemia of women with polycystic ovary syndrome. Elucidating the pathogenesis of metabolic syndrome should promote the initiation of novel therapeutic approaches.

Keywords: stress,hypothalamic-pituitary-adrenocortical axis,metabolic syndrome,cortisol secretion,adrenergic stimulation,visceral obesity,free fatty acids,polycystic ovary syndrome

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How to cite
Brudaşcă I, Cucuianu M. Chronic Stress, Neuroendocrine Disorders and Metabolic Syndrome. Rev Romana Med Lab. 2011;19(3):219-26