PMID- 16298496
OWN - NLM
STAT- MEDLINE
DCOM- 20060622
LR  - 20220321
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 66
IP  - 3
DP  - 2006
TI  - Metabolic syndrome--neurotrophic hypothesis.
PG  - 545-9
AB  - 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.
FAU - Hristova, M
AU  - Hristova M
AD  - Varna University of Medicine, Department of Endocrinology, 17 Mur St., Entr. 2, 
      BG - 9003 Varna, Bulgaria. library@io-bas.bg
FAU - Aloe, L
AU  - Aloe L
LA  - eng
PT  - Journal Article
DEP - 20051118
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
CIN - Med Hypotheses. 2006;67(1):195-6. PMID: 16545915
MH  - Adult
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Humans
MH  - Inflammation
MH  - Interleukin-6/metabolism
MH  - Lipid Metabolism
MH  - Metabolic Syndrome/*diagnosis/*pathology
MH  - Middle Aged
MH  - Models, Biological
MH  - Models, Theoretical
MH  - Nerve Growth Factor/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2005/11/22 09:00
MHDA- 2006/06/23 09:00
CRDT- 2005/11/22 09:00
PHST- 2005/08/23 00:00 [received]
PHST- 2005/08/31 00:00 [accepted]
PHST- 2005/11/22 09:00 [pubmed]
PHST- 2006/06/23 09:00 [medline]
PHST- 2005/11/22 09:00 [entrez]
AID - S0306-9877(05)00477-9 [pii]
AID - 10.1016/j.mehy.2005.08.055 [doi]
PST - ppublish
SO  - Med Hypotheses. 2006;66(3):545-9. doi: 10.1016/j.mehy.2005.08.055. Epub 2005 Nov 
      18.