Effect of high doses of synthetic estrogen on lipid metabolism in castrated male rats |
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Authors: | M Nishikawa K Seki Y Matsuzawa Y Minami S Kawata S Miyoshi Y Imai R Saitoh S Noda S Tamura S Tarui |
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Affiliation: | (1) The Second Department of Internal Medicine, Osaka University Medical School, Fukushima, Fukushima-ku, 553 Osaka, Japan |
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Abstract: | The mechanism by which high doses of estrogen influences lipid metabolism was studied with a microtubular blocking agent.
Castrated male rats received oral injection daily for 14 days of 3 mg hexestrol in olive oil, or oil alone as controls. About
half of the animals in each group were injected intraperitoneally with 4 mg/100 g body weight colchicine 3 hr before they
were killed. Hexestrol treatment caused an accumulation of esterified cholesterol in the liver while it decreased those in
serum. Triglyceride concentrations slightly decreased in the liver but were unaffected in serum. On polyacrylamide-gel disc
electrophoresis, the peaks of high density lipoproteins (HDL) and low density lipoproteins (LDL) were decreased remarkably.
Electron microsopic examination of hepatocytes revealed electron-lucent lipid droplets in the cytoplasm.
After a colchicine treatment of the control animals, concentrations of esterified cholesterol and triglycerides markedly increased
in the liver, while those in serum decreased. Electron microscopic examination of hepatocytes revealed numerous secretory
vesicles filled with nascent VLDL. In hexestrol-treated animals, the colchicine treatment was associated with marked decreases
in serumesterified cholesterol and triglyceride as seen in the controls. However, there were no further increases of esterified
cholesterol in the liver, and the increase of triglycerides was slight. Electron microscopic examination showed less secretory
droplets than in the controls.
These data suggest that very low density lipoproteins (VLDL) synthesis in the liver of hexestrol treated rats was inhibited.
An accumulation of esterified cholesterol with a marked decrease in serum could not be accounted for by the inhibition of
lipoproteins secretion, but rather by their enhanced entry into the liver. |
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