title: The correlations between endogenous dehydroepiandrosterone sulfate and some atherosclerosis risk factors in premenopausal women.
abstract: BACKGROUND
  Dehydroepiandrosterone (DHEA) is postulated to have antiatherogenic properties, but the possible mechanism of this action is unclear. The aim of this study was to determine the influence of endogenous DHEA-S on the levels of some factors playing significant roles in atherogenesis.
  
  
  METHODS
  In a group of 40 premenopausal women, relationships between endogenous DHEA-S and serum lipids and the apolipoproteins A1 (apoA1) and B (apoB), serum lipid peroxide (LPO), and total antioxidant system (TAS) concentrations as markers of the serum antioxidant-prooxidant balance were measured as well as clinical and biochemical parameters playing roles in atheromatosis such as the type of obesity and the serum glucose, insulin, insulin-like growth factor (IGF-1) and homocysteine (HCY) concentrations.
  
  
  RESULTS
  Statistical analysis revealed significant correlation (p<0.05) between serum DHEA-S level and the serum concentrations of: HDL(2)-C (r=0.53), HDL(2)-C/HDL(3)-C (r=0.58), TG (r=0.35), IGF-1 (r=0.39), and HCY (r=-0.44). There was no statistically significant correlation between DHEA-S level and other biochemical and clinical parameters (age, BMI, WHR) found in this study.
  
  
  CONCLUSIONS
  Despite unfavorable correlation between DHEA-S and TG concentration, the results of this study indicate a potential antiatherogenic action of DHEA which may occur through various mechanisms: by increasing HDL(2)-C and the HDL(2)-C/HDL(3)-C ratio, which has an atheroprotective effect, by elevating the serum IGF-1 concentration, or by decreasing the HCY level. These preliminary results, however, require further investigation.
authors.affiliation: Department of Endocrinology, Diabetology, and Isotope Treatment, Medical University of Wrocław, Wrocław, Poland. tupikowska@epf.pl
authors.forename: Grazyna
authors.initials: G
authors.lastname: Bednarek-Tupikowska
authors.forename: Urszula
authors.initials: U
authors.lastname: Tworowska-Bardzińska
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Tupikowski
authors.forename: Anna
authors.initials: A
authors.lastname: Bohdanowicz-Pawlak
authors.forename: Jadwiga
authors.initials: J
authors.lastname: Szymczak
authors.forename: Eliza
authors.initials: E
authors.lastname: Kubicka
authors.forename: Anna
authors.initials: A
authors.lastname: Skoczyńska
authors.forename: Andrzej
authors.initials: A
authors.lastname: Milewicz
mesh_terms: D050197:Atherosclerosis / Q000097:blood* / Q000209:etiology*; D001786:Blood Glucose / Q000378:metabolism; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008875:Middle Aged; D017697:Premenopause / Q000097:blood*; D012307:Risk Factors
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D006710:Homocysteine; D019314:Dehydroepiandrosterone Sulfate; D007334:Insulin-Like Growth Factor I