Metabolic syndrome – Neurotrophic hypothesis. (Articolo in rivista)

  • Metabolic syndrome – Neurotrophic hypothesis. (Articolo in rivista) (literal)
  • 2006-01-01T00:00:00+01:00 (literal)
Alternative label
  • Hristova M.1, Aloe L.2 (2006)
    Metabolic syndrome – Neurotrophic hypothesis.
    in Medical hypotheses
  • Hristova M.1, Aloe L.2 (literal)
Pagina inizio
  • 545 (literal)
Pagina fine
  • 549 (literal)
  • Impact Factor = 1.299 (literal)
  • 66/3 (literal)
  • ISI Web of Science (WOS) (literal)
  • 1 = Varna University of Medicine, Department of Endocrinology, 17 Mur St., Entr. 2, BG – 9003 Varna, Bulgaria; 2 = Institute of Neurobiology and Molecular Medicine, Rome, Italy. (literal)
  • Metabolic syndrome – Neurotrophic hypothesis. (literal)
  • An increasing number of researchers of the metabolic syndrome assume that many mechanisms are involved in its complex pathophysiology such as an increased sympathetic activity, disorders of the hypothalamo-pituitary-adrenal axis, the action of chronic subclinical infections, proinflammatory cytokines, and the effect of adipocytokines or psychoemotional stress. An increasing body of scientific research in this field confirms the role of the neurotrophins and mastocytes in the pathogenesis of inflammatory and immune diseases. Recently it has been proved that neurotrophins and mastocytes have metabotrophic effects and take part in the carbohydrate and lipid metabolism. In the early stage of the metabolic syndrome we established a statistically significant increase in the plasma levels of the nerve growth factor. In the generalized stage the plasma levels of the neutrophines were statistically decreased in comparison to those in the healthy controls. We consider that the neurotrophin deficit is likely to play a significant pathogenic role in the development of the metabolic anthropometric and vascular manifestations of the generalized stage of MetSyn. We suggest a hypothesis for the etiopathogenesis of the metabolic syndrome based on the neuro-immuno-endocrine interactions. The specific pathogenic pathways of MetSyn development include: (1) increased tissue and plasma levels of proinflammatory cytokines Interleukin-1(IL-1), Interleukin-6 (IL-6 ) and tumor necrosis factor - alpha (TNF-alpha) caused by inflammatory and/or emotional distress; (2) increased plasma levels of neurotrophin - nerve growth factor (NGF) caused by the high IL-1, IL-6 and TNFalpha levels; (3) high plasma levels of NGF which enhance activation of: the autonomous nerve system--vegetodystonia (disbalance of neurotransmitters); Neuropeptide Y (NPY)--enhanced feeding, obesity and increased leptin plasma levels; hypothalamo-pituitary-adrenal axis--increased corticotropin-releasing hormone (CRH) and cortisol (hormonal disbalance); immune cells--increased number and degranulation of mastocytes (MC)--immunological disbalance; (4) as a result of 1-3 insulin resistance is exhibited leading to diabetes mellitus. The hypothesis is confirmed by results obtained after 6-month nonsteroid anti-inflammatory treatment of patients with MetSyn. These results are reported in a separate publication. (literal)
Prodotto di
Autore CNR

Incoming links:

Autore CNR di