title: [Oxidation stress, insulin resistance and endothelial dysfunction during the treatment of hyperlipidaemia].
abstract: BACKGROUND
  Hyperlipidaemia represents one of the major risk factors of the type 2 diabetes mellitus (DM2). In the pathogenesis of insulin resistance (IR) development glucose homeostasis impairment and their progression into DM2, oxidative stress and endothelial dysfunction (ED) may play an important role. Recent papers indicate the possibility to prevent the development of DM2 by HLP treatment, which is characterised by increased oxidation stress and ED.
  
  
  RESULTS
  For the period of twelve months 46 patients with primary HLP (group S) (LDL-C > 4.1 mmol/l a TG < 3.5 mmol/l), were treated with atorvastatine 20 mg or simvastatine 40 mg. Patients with LDL-C > 4.1 mmol/l along with TG > 3.5 mmol/l were randomly divided into two groups. The SF group was treated with a combination of statin + 200 mg micronized fenofibrate each day, and group SR received together with statin a compound containing n-3 polyene fatty acids (PUFA n-3) in the daily dose of 3.6 g. After one year lasting therapy we found beside the positively influenced concentration of atherogenic lipids and lipoproteins in the group S and SF a significantly reduced concentration of conjugated dienes (CD) in LDL ( -21, resp. 16%, both P < 0.05); the test of KD kinetics in LDL in the group S has marginal increase of the lag phase (P = 0.06) and in the groups S and SR also a significant improvement of ED (increase by the flow of mediated vasodilation, FMD) by 20%, resp. by 18% (both P < 0.05) and in the SR group a significant decrease of microalbuminuria. We did not proved significant concentrations of insulin, C-peptide or indexes showing the degree of IR (HOMA and QUICKI) CONCLUSIONS: Long-lasting hypolipidemic treatment positively affected in our study the oxidative stress and ED, however, it did not resulted in changes of IR.
authors.affiliation: IV. Interní klinika 1. LF UK a VFN, Praha. zemanm@vfn.cz
authors.forename: M
authors.initials: M
authors.lastname: Zeman
authors.forename: M
authors.initials: M
authors.lastname: Vecka
authors.forename: P
authors.initials: P
authors.lastname: Stopka
authors.forename: M
authors.initials: M
authors.lastname: Zahin
authors.forename: E
authors.initials: E
authors.lastname: Tvrzická
authors.forename: B
authors.initials: B
authors.lastname: Stanková
authors.forename: T
authors.initials: T
authors.lastname: Vareka
authors.forename: L
authors.initials: L
authors.lastname: Janíková
authors.forename: A
authors.initials: A
authors.lastname: Zák
mesh_terms: D000328:Adult; D000368:Aged; D000069059:Atorvastatin; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D015525:Fatty Acids, Omega-3 / Q000627:therapeutic use; D005260:Female; D011345:Fenofibrate / Q000627:therapeutic use; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011758:Pyrroles / Q000627:therapeutic use; D019821:Simvastatin / Q000627:therapeutic use
chemical_list: D015525:Fatty Acids, Omega-3; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D011758:Pyrroles; D000069059:Atorvastatin; D019821:Simvastatin; D011345:Fenofibrate