Neuro-Endocine Alterations in Metabolic Syndrome
Author: Robeva, Ralitsa N., Milcheva, Bojka A., Elenkova, Atanaska P. , Zacharieva, Sabina Z.
Clinical Center of Endocrinology and Gerontology, USHATE “Acad. Iv. Penchev”, Medical Faculty, Medical University, Sofia
An important role of chronic stress for the body energy balance and adipocyte growth has long been assumed, but precise pathophysiological mechanisms are still unknown. Adaptive stress response is mainly regulated by the hypothalamic-pituitary-adrenal axis and the autonomic nervous system, which both ensure the adequate body protection and maintenance of normal homeostasis. However, under chronic stress, the same adaptive mechanisms might induce neuroendocrine and behavioral changes that could potentiate the onset of metabolic abnormalities.
The present review is focused on the scientific data examining cortisol secretion disturbances in visceral obesity and metabolic syndrome (MS), as well as the discrepancies between published studies. The role of the sympathetic
nervous system and adrenal medulla is also considered. Studies have shown that reduced hypothalamic-pituitary adrenal axis plasticity could favor the development of MS but the possible interactions are likely to be modulated
by a plenty of other factors such as age, gender, concomitant medication, chronic stress, bad habits, ethnicity and socio-economic affiliation.
It is probable that the sympathetic hyperactivity as well as the reduced adrenal catecholamine secretion might be other important factors facilitating the development of metabolic imbalance. Unfortunately, literature data considering interactions between the two main adaptive systems are scarce, thus, the need for additional research is urgent. Revealing the associations between the neuroendocrine system and metabolic abnormalities might help to clarify the pathophysiology of MS as well as the development of future therapeutic strategies allowing a more successful adaptation to chronic stress.
Key words: metabolic syndrome, cortisol, catecholamines, stress