Arteriosclerosis and Thrombosis, Vol 11, 1719-1729, Copyright © 1991 by American Heart Association

ARTICLES

Effect of corn and coconut oil-containing diets with and without cholesterol on high density lipoprotein apoprotein A-I metabolism and hepatic apoprotein A-I mRNA levels in cebus monkeys

AF Stucchi, LK Hennessy, DB Vespa, EJ Weiner, J Osada, JM Ordovas, EJ Schaefer and RJ Nicolosi
Department of Clinical Sciences, University of Lowell, MA 01854.

The mechanism(s) by which diets containing corn or coconut oil (31% of energy as fat) totally free of cholesterol or with 0.1% added cholesterol by weight (0.3 mg/kcal) affect plasma high density lipoprotein cholesterol (HDL-C), apoprotein (apo) A-I levels, apo A-I kinetics, and hepatic apo A-I mRNA concentrations were investigated in 26 cebus monkeys. Coconut oil-fed monkeys had elevated levels of plasma total cholesterol (217%), very low density lipoprotein plus low density lipoprotein cholesterol (331%), HDL-C (159%), and apo A-I (117%) compared with corn oil-fed animals. Although the addition of cholesterol to the corn oil diet significantly increased these parameters, no such effects were seen when cholesterol was added to the coconut-oil diet. Both the type of fat and cholesterol in the diet significantly affected HDL apo A-I metabolism by decreasing apo A-I fractional catabolic rate and increasing apo A-I production rate in the coconut oil-fed groups. The decrease in apo A-I fractional catabolic rate in the coconut oil-fed animals was also associated with an increase in the HDL core lipid to surface ratio. Liver apo A-I mRNA abundance was elevated in the coconut oil-fed groups; however, dietary cholesterol had no affect on these levels. The lack of parallel effects of dietary fat and cholesterol on apo A-I production rate and liver apo A-I mRNA levels suggests that the increase in the apo A-I production rate observed in the coconut oil-fed groups resulted from the fat- induced rise in liver apo A-I mRNA abundance, whereas the cholesterol- induced rise in the apo A-I production rate resulted from a mechanism other than changes in liver apo A-I mRNA levels.

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