Mechanism of hyperlipidemia produced by estrogen-progestin formulation.
Rats administered estrogen-progestin formulation (0.667 mg of synthetic progestin and 0.067 mg of synthetic estrogen/kg body wt) showed increased hepatic cholesterogenesis, as evidenced by an increased activity of HMG-CoA reductase and increased incorporation of labelled acetate into liver cholesterol. Hepatic degradation of cholesterol to bile acids, however, was decreased. There was increased release of lipoproteins into the circulation but their clearance from the circulation was lower as revealed by a decreased activity of lipoprotein lipase of the extrahepatic tissues. Activity of plasma LCAT, which is involved in the transport of cholesterol from the tissues, was also decreased. The increase in serum and aortic cholesterol levels, increase in LDL cholesterol and decrease in HDL cholesterol in rats administered estrogen-progestin formulation suggest that prolonged administration of this formulation may predispose towards atherosclerosis.
Sissan
M A
MA
Department of Biochemistry, University of Kerala, Trivandrum.
Leelamma
S
S
D000818:Animals; D003276:Contraceptives, Oral; D004967:Estrogens; D005260:Female; D006949:Hyperlipidemias / Q000097:blood / Q000139:chemically induced*; D011372:Progestins; D051381:Rats; D011919:Rats, Inbred Strains
D003276:Contraceptives, Oral; D004967:Estrogens; D011372:Progestins