The aim of the present study was to evaluate the effect of leptin hormone and
Gemfibrozil on the body weight, hepatic & serum lipids and lipoproteins profile in
ethanol-induced hyperlipidemia in rats. The study was carried on 53 male albino rats
weighing 130-160 g classified into six groups (from A-F). Three of these groups were
fed a normal diet (A, C and D), while the other groups (B, E and F) were fed a
normal diet combined with ethanol (6.32 g/kg body weight per oral) for the first 30
days. Subsequently, the first three groups received a normal diet for group (A), in
addition to Gemfibrozil (100 mg/kg per oraldaily) for group (C) or exogenous leptin
(230 µg/kg body weight, i.p.) every alternate day for group (D), while Groups (E) and
(F) were administered Gemfibrozil and leptin respectively for the next 15 days. At the
end of the total experimental period of 45 days, liver total lipids, serum
concentrations of total cholesterol, HDL-C, LDL-C, VLDL-C, triglycerides, total
proteins, albumin and glucose were measured. Ethanol-induced hyperlipidemia in
rats resulted in marked increase of liver total lipids and significantincrease of serum
total cholesterol, LDL-C, VLDL-C and triglycerides levels. This was associated with
concomitant decrease in serum HDL-cholesterol and glucose levels as well as serum
total proteins and albumin levels. However, no changes were observed in the body
weight gain. Administration of leptin or Gemfibrozil separately or after ethanol-induced hyperlipidemia to rats was able to antagonize the ethanol-induced
biochemical changes in the tissues studied. The results of the current study showed
that leptin administered alone to rats resulted in marked decrease of their body
weight and fasting serum glucose levels while serum HDL-C was elevated. These
findings indicated that the chronic administration of exogenous leptin was more
effective as compared to Gemfibrozil in preventing the rise in lipids and lipoproteins
concentration in an animal model of alcohol-induced hyperlipidemia.