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AJP - Endocrinology and Metabolism, Vol 258, Issue 1 E172-E183, Copyright © 1990 by American Physiological Society
ARTICLES |
R. S. Kushwaha, D. M. Foster, P. H. Barrett and K. D. Carey
Department of Physiology and Medicine, Southwest Foundation for Biomedical Research, San Antonio, Texas 78284.
To determine the metabolic mechanisms by which estrogen and progesterone alter levels of apoprotein B (apo B)-containing lipoproteins, 12 ovariectomized and hysterectomized baboons, maintained on a high-cholesterol (1.7 mg/kcal) and a high-fat (40% from lard) diet and divided into four groups, were treated with estrogen, progesterone, estrogen plus progesterone, and a placebo. After 12 wk, plasma cholesterol was unchanged in the control and progesterone groups but was reduced in the estrogen- and estrogen plus progesterone-treated groups. The reduction was primarily because of decreased low-density lipoprotein (LDL) cholesterol. LDL apo B levels decreased parallel to the LDL cholesterol. Very low-density lipoprotein (VLDL) and LDL apo B metabolism were studied using a double-label turnover study. Multicompartmental modeling suggested that LDL apo B was kinetically heterogeneous and that there exists an extravascular pool, perhaps consisting of hepatic remnants, that contributes significantly to LDL apo B transport. The model was used to estimate apo B production rates and residence times. VLDL apo B production was not affected by estrogen but was increased by progesterone. LDL apo B production was increased by both estrogen and progesterone. The residence time of LDL apo B was decreased by estrogen and estrogen plus progesterone but not by progesterone. Thus estrogen and progesterone have independent effects on apo B metabolism in baboons.
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