Effect of ciprofibrate on lipoprotein metabolism and oxidative stress parameters in patients with type 2 diabetes mellitus and atherogenic lipoprotein phenotype

Citation
K. Raslova et al., Effect of ciprofibrate on lipoprotein metabolism and oxidative stress parameters in patients with type 2 diabetes mellitus and atherogenic lipoprotein phenotype, ACT DIABETO, 37(3), 2000, pp. 131-134
Citations number
17
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ACTA DIABETOLOGICA
ISSN journal
09405429 → ACNP
Volume
37
Issue
3
Year of publication
2000
Pages
131 - 134
Database
ISI
SICI code
0940-5429(200009)37:3<131:EOCOLM>2.0.ZU;2-H
Abstract
The effect of ciprofibrate therapy on plasma lipids and lipoproteins, HDL a nd LDL subfraction profile, fractional esterification rate of HDL cholester ol (FERHDL) and the resistance of LDL and serum lipids to oxidation was stu died in 24 males with type 2 diabetes and atherogenic lipoprotein phenotype (ALP). We also examined the effect of ciprofibrate therapy on oxidative DN A damage in peripheral lymphocytes. No differences in glucose, HbA1C and BM I levels were found after three months of ciprofibrate therapy. Ciprofibrat e significantly decreased total cholesterol and triglyceride levels by 5.5% and 50% (p = 0.05; 0.001, respectively) and increased HDL-cholesterol leve ls by 8.5% (p = 0.05). FERHDL and LDL subfraction profile were also favorab ly affected. However, no effect on HDL subclasses was found. There were no statistically significant differences in lipid resistance to oxidation meas ured in serum and in LDL (lag time and V-max) before and after therapy. No significant effect of ciprofibrate was found on oxidative DNA damage. The e valuation of the relationship between oxidative damage of purines with lag time in LDL and maximal rate of serum lipid oxidation showed significant co rrelations after therapy (r = -0.58; 0.47, p = 0.01; 0.05, respectively), b ut only trends before starting ciprofibrate treatment. Type 2 diabetes mell itus represents a complex metabolic disorder expressed in glucose and lipop rotein disturbances and increased oxidative stress. Ciprofibrate therapy fa vorably affected major features of lipid abnormalities of diabetic patients , but the level of oxidative stress assessed by in vitro and in vivo method s was not changed. The evaluation of expected logical correlations between the parameters of lipoprotein metabolism, lipid resistance in serum and LDL , and oxidative DNA damage showed that those correlations were more relevan t and significant after ciprofibrate treatment and were not related with gl ucose homeostasis.