Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/55124
Type: Artigo de periódico
Title: Atherosclerosis is enhanced by testosterone deficiency and attenuated by CETP expression in transgenic mice
Author: Casquero, AC
Berti, JA
Salerno, AG
Bighetti, EJB
Cazita, PM
Ketelhuth, DFJ
Gidlund, M
Oliveira, HCF
Abstract: In this work, we investigated the impact of testosterone deficiency and cholesteryl ester transfer protein (CETP) expression on lipoprotein metabolism anddietinduced atherosclerosis. CETP transgenic mice and nontransgenic (nTg) littermates were studied 4 weeks after bilateral orchidectomy or sham operation. Castrated mice had an increase in the LDL fraction (136% for CETP and 179% for nTgmice), whereas the HDL fraction was reduced (230% for CETP and -11% for nTg mice). Castrated mice presented 1.7-fold higher titers of anti-oxidized LDL (Ox-LDL) antibodies than sham-operated controls. Plasma levels of CETP, lipoprotein lipase, and hepatic lipase were not changed by castration. Kinetic studies showed no differences in VLDL secretion rate, VLDL-LDL conversion rate, or number of LDL and HDL receptors. Competition experiments showed lower affinity of LDL from castrated mice for tissue receptors. Diet-induced atherosclerosis studies showed that testosterone deficiency increased by 100%, and CETP expression reduced by 44%, the size of aortic lesion area in castrated mice. In summary, testosterone deficiency increased plasma levels of apolipoprotein B-containing lipoproteins (apoB-LPs) and anti-OxLDL antibodies, decreased LDL receptor affinity, and doubled the size of diet-induced atherosclerotic lesions. The expression of CETP led to a milder increase of apoB-LPs and reduced atherosclerotic lesion size in testosterone-deficient mice.
Subject: low density lipoprotein receptor
lipoprotein lipase
lipolysis
plasma lipoprotein kinetics
oxidized low density lipoprotein
aortic atherosclerosis lesion
cholesteryl ester transfer protein
Country: EUA
Editor: Amer Soc Biochemistry Molecular Biology Inc
Rights: fechado
Identifier DOI: 10.1194/jlr.M600135-JLR200
Date Issue: 2006
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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