title: [Serum concentrations of tumor necrosis factor TNFalpha and its soluble receptors in obese women with diabetes type 2 and without additional disease].
abstract: BACKGROUND
  TNF-alpha is one with mediators insulin resistance. Previous study showed, that in obesity there is an increased synthesis of TNF-alpha by fat cells and serum concentrations of TNF-alpha. The aim of present study was: 1. To assess of serum concentrations of TNF-alpha and TNF soluble receptors sTNFRs in obese women with diabetes type 2 and obese women without additional disease. 2. To assess possible association between of manner treatment of diabetes type 2 and serum concentrations of TNF-alpha and TNF soluble receptors.
  
  
  METHODS
  The study group's involved 23 obese women with diabetes type 2 - group A (age 63.6 +/- 8.2 lat; BMI 32.7 +/- 3,9 kg/m2) in this 12 treated of derivatives of sulfonylurea (age 65.1 +/- 6.6 lat; BMI 32.0 +/- 3.4 kg/m2) - subgroup AI and 11 insulin treated (age 62.1 +/- 9.7 lat; BMI 33.4 +/- 4.4 kg/m2) - subgroup AII and 23 obese women without additional disease and without any pharmacological treatment - group B (age 36.6 +/- 10.9 lat; BMI 36.6 +/- 5.6 kg/m2). Body weight and height were measured, body mass index was calculated with formula. Serum concentrations of glucose was measured by enzymatic procedure. Serum concentrations of TNF-alpha and it's soluble receptors sTNFR1 and sTNFR2 was measured by ELISA. and sTNFR2 were significant decreased (respectively p <0,005 i p <0,001) in group A when compared to group B. There are not significant differences serum concentration of TNF-alpha and its soluble receptors between subgroups AI and AII.
  
  
  CONCLUSIONS
  1. In obese women with diabetes type 2 serum concentration of TNF-alpha increased and concentrations of its soluble receptors decreased when compared to obese without additional disease. 2. The treatment meaner of diabetes type 2 not influence of serum concentration of TNF-alpha and sTNFR1 but application of insulin maybe a cause increase activity sTNFR2.
authors.affiliation: Department of Pathophysiology Medical University of Silesia. magols@esculap.pl
authors.forename: Magdalena
authors.initials: M
authors.lastname: Olszanecka-Glinianowicz
authors.forename: Iwona
authors.initials: I
authors.lastname: Waluszek-Kończakowska
authors.forename: Barbara
authors.initials: B
authors.lastname: Zahorska-Markiewicz
authors.forename: Joanna
authors.initials: J
authors.lastname: Janowska
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000150:complications; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood*; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood*; D018709:Statistics, Nonparametric; D013453:Sulfonylurea Compounds / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D007328:Insulin; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D013453:Sulfonylurea Compounds; D014409:Tumor Necrosis Factor-alpha