Hyperleptinemia is considered to be one of predictors of early atherosklerosis complications. This stimulated us to investigate differences between leptinemia in persons with accelerated
atherosclerosis and leptinemia in probands without
atherosclerosis complications. The study also verified whether leptinemia and its relationship to other anthropometric and biochemical parameters can differ in hypolipemic-treated probands and hypolipemic-untreated individuals. We examined 89 probands with accelerated
atherosclerosis. The controls were 20 persons without any signs of accelerated
atherosclerosis. Probands with accelerated
atherosclerosis had a slight
hyperglycemia and were slightly obese, but they did not meet criteria of
metabolic cardiovascular syndrome. No significant differences between both groups under study were found in terms of anthropometric and biochemical parameters (BMI, % body fat, glycemia,
insulin,
C-peptide, intact
proinsulin, total
proinsulin cholesterol, HDL,
triglycerides,
LDL, homeostatic model of insulin secretion and resistance).
Leptin concentration was not different as well. Stratification into males and females showed that women had a significantly higher leptinemia and fat tissue mass. Other biochemical parameters were similar in both groups. We suppose that in individuals without signs of
metabolic syndrome, leptinemia does not belong among predictors of accelerated
atherosclerosis. The accelerated
atherosclerosis persons were then divided into subgroups according to medication (28 probands--
pravastatin Lipostat 20, 15 probands--
phenofibrate Lipanthyl 200M, 9 probands--
simvastatin Zocor 20, 47 probands--no hypolipemic medication). No significant differences between the groups were found in terms of the analysed anthropometric and biochemical parameters, except leptinemia. The
pravastatin-medicated probands had a significantly lower leptinemia (significant at 99% significance level) which was evidently sex-related than other patients. The
pravastatin-administered persons showed no correlation between leptinemia and body fat mass (in contrast to other groups where such a correlation was highly statistically significant). These findings can be explained by a still unclear effect of
pravastatin on
insulin metabolism and on other factors involved in
leptin synthesis and elimination. Thus, a new
therapeutic effect of
pravastatin can be supposed. This may account for a highly favourable effect of
pravastatin on reduced manifestations of
atherosclerosis complications event at a low
LDL cholesterol decrease (particularly in persons with
metabolic cardiovascular syndrome).