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FNO and adiposity

As have shown researches of last years, the fatty tissue possesses auto - a para-and endocrine function and cosecretes a considerable quantity of the substances possessing various biological effects which can cause development of complications accompanying adiposity including insulinorezistentnosti [87,199].

The important role in development and advance insulinorezistentnosti is played by a visceral fatty tissue [215]. Experimental and clinical researches with klemp-method use have shown direct dependence between degree of development of an is abdominal-visceral fatty tissue and expression insulinorezistentnosti [74].

The intensive lipolysis in visceral adipotsitah leads to allocation of a considerable quantity of free fat acids (SZHK), mainly in portal circulation and a liver. In liver SZHK interfere with linkage of insulin by hepatocytes, causing development insulinorezistentnosti at liver level, depression of secretion of insulin by a liver and development system giperinsulinemii [124,208].

Last years the role of a cytokine FNO in an adiposity pathogenesis is intensively studied. Two kinds bound to a fatty tissue adipotsitokinov are known: true - adiponektin and leptin, and cytokines not specific to a fatty tissue, such as interlejkin-6, the transforming factor of growth-r, ingibitor-1 the activator plazminogena, an angiotensinogen and FNO [114,146].

C modern positions FNO it is surveyed as biologically active cytokine which co-ordinates functional interrelations between a fatty tissue and insulinochuvstvitelnymi organs and tissues [130,70]. FNO stimulates a lipolysis in a fatty tissue, production of free fat acids, regulates an expression of genes of enzymes and hormones which induce media even signals of insulin [121,171].

Many researchers survey the TNF-ALPHA, as a mediator insulinorezistentnosti at adiposity [170]. Expression ФНО-a more all is expressed in adipotsitah to a visceral fatty tissue. ФНО-a reduces activity tirozinkinazy an insulinic receptor and fosforilirovanie Thyrosinum of substrate of an insulinic receptor, and also brakes an expression of intracellular carriers of glucose ГЛЮТ-4 in a muscular and fatty tissue [152,174]. As shown in vivo, ФНО-a can operate in a synergy with other cytokines cosecreted adipotsitami - interlejkinami-1 and 6, and also to stimulate secretion leptina [212].

In culture of cells adipotsitov it has been shown, that the long incubation with ФНО-a reduces level mrnk on 85-90 %, and level mrnk insulinic receptors decreases on 50 % (Stephens et al., 1994). Probably, important role in this process is played by one of transkriptsionnyh factors. Guo, Donner et al. (1996) have found out a duality of effects ФНО-a on adipotsity in culture of cells. At short-term incubation ФНО-a potentsiiruet effects of insulin: amplifies fosforilirovanie ИРС-1, linkage with р85 reguljatornoj subedinitsej PI-3 kinazy and it fosforilirovanie is facilitated. However at an incubation adipotsitov within 5 days about 0,1 nanometers ФНО-a effects of this fiber become opposite: there is a reduction fosforilirovanija P -

subedinitsy an insulinic receptor and ИРС-1 [104]. Studying influence FNO - an on insulinic receptors in adipotsitah, Gual, Valverde et al. Have shown, that the incubation with ФНО-a is negatively reflected in processes fosforilirovanija an insulinic receptor, but does not influence in any way the general number of receptors and their molecular mass [162,181,102].

The big role in adiposity development take away to local rising of level ФНО-a. Adipotsity at patients with adiposity produce superfluous quantity ФНО-a, and its level positively correlates with an index of mass of a body (IMT) and giperinsulinemiej [94,171]. Knjazeva L.I., etc., have taped, that at patients with IMT more than 30 kg/m in comparison with

By patients with IMT, not exceeding 25 kg/m, level FNO in a fatty tissue it is enlarged in 2,5 times, and depression of mass of a body by 17 % from initial IMT it is bound to depression FNO on 45 %. The highest level FNO was defined at patients with II - III degree of adiposity. At very full patients (IMT 45 kg/m there are more) level FNO was more low, than at adiposity II - III degrees. Studying polymorphism of a gene FNO, Lui J. et al have found out, that homozygotes on G-allelju with adiposity reduce body mass, than carriers I-allelja more effectively. At a weight loss on 26,6 % from initial weight there is an authentic depression FNO approximately on 58 % from the initial. At adiposity FNO plays the leading part in activation of others adipotsitokinov, in particular, raises synthesis of an inhibitor of the activator plazminogena-1 [84].

In researches in vivo, FNO can operate in a synergy with other cytokines cosecreted adipotsitami - interlejkinami-1 and 6, and also to stimulate secretion leptina. It is shown, that after an incubation hypodermic adipotsitov with FNO tranzitorno levels leptina and lipoproteinlipazy bloods (Fried S.K increase., Zechner R. 1989).

In a number of researches it has been shown, that high level of a cytokine FNO in blood and an expression of its receptors in a fatty tissue repeatedly increases at adiposity [82]. The presented data allow to survey FNO, as a mediator insulinorezistentnosti at adiposity [70,176].

1.5.

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A source: SEREBRYAKOVA Oksana Evgenevna. INTERRELATION of POLYMORPHISM of the GENE of the FACTOR of the NECROSIS of the TUMOUR the ALPHA With RISK of DEVELOPMENT of the METABOLIC SYNDROME And the ATHEROSCLEROSIS. The dissertation on competition of a scientific degree of the candidate of medical sciences. Moscow -. 2014

More on topic FNO and adiposity:

  1. Adiposity
  2. FNO and disturbances of a lipide exchange
  3. FNO and carbohydrate metabolism disturbances
  4. FNO, an atherosclerosis and cardiovascular diseases
  5. FNO and transfer of an insulinic signal
  6. 3.1. DYNAMICS of CLINICAL INDICATORS At PATIENTS Taking into account POLYMORPHISM of the GENE FNO
  7. 3.3. The ANALYSIS of INDICATORS of CARBOHYDRATE METABOLISM At PATIENTS Taking into account POLYMORPHISM of the GENE FNO
  8. 3.2. DYNAMICS of INDICATORS of the LIPIDE SPECTRUM At PATIENTS Taking into account POLYMORPHISM of the GENE FNO
  9. the Table of contents
  10. Chapter 4. Discussion of the received results
  11. PRACTICAL REFERENCES
  12. 4.1. Интерлейкин-1 r, the factor of a necrosis of a tumour and and interferon at at an undifferentiated dysplasia of a connecting tissue
  13. PRACTICAL REFERENCES
  14. Knowledge of the woman and the medical control in aspect gravidarnogo augmentations of mass of a body
  15. the literature List
  16. CONCLUSIONS
  17. Patients
  18. 3.1.1 Formation of a metabolic syndrome
  19. Features of a carbohydrately-fatty exchange at patients with various mass of a body
  20. Socially-demographic and medicobiological factors GUMT