Gr. Xu et al., Campestanol (24-methyl-5 alpha-cholestan-3 beta-ol) absorption and distribution in New Zealand white rabbits: Effect of dietary sitostanol, METABOLISM, 48(3), 1999, pp. 363-368
Campestanol (24-methyl-5 alpha-cholestan-3 beta-ol) is a naturally occurrin
g plant stanol, structurally similar to cholesterol (5-cholesten-3 beta-ol)
and widely distributed in vegetable oils consumed in human diets. We measu
red the absorption and turnover of campestanol by the plasma dual-isotope r
atio method and mathematical analysis of specific activity versus time deca
y curves after simultaneous oral and intravenous pulse-labeling with [3 alp
ha-H-3]- end [23-C-14]-labeled campestanol, respectively, in New Zealand Wh
ite (NZW) rabbits: six fed chow and six fed chow with 125 mg/d campestanol
end 175 mg/d sitostanol (24-ethyl-5 alpha-cholestan-3 beta-ol). Plasma conc
entrations increased insignificantly from 0.08 +/- 0.01 to 0.09 +/- 0.01 mg
/dL with dietary stanols. The percent campestanol absorption measured by th
e plasma dual-isotope ratio method after the rabbits were fasted for 6 hour
s yielded the percent absorption in the absence of competing intestinal ste
rols and stanols and declined insignificantly from 11.6% +/- 3.5% in contro
ls to 8.1% +/- 3.7% in the treated rabbit groups. In contrast, the turnover
, which measured actual absorption averaged over 24 hours, increased from 0
.12 +/- 0.05 to 0.37 +/- 0.05 mg/d (P < .05) with campestanol and sitostano
l added to the diet. However, the actual percent absorption declined from 3
% to 0.3% of dietary intake with the campestanol and sitostanol-enriched di
et. Campestanol pool sizes, although remaining small, increased slightly fr
om 1.1 +/- 0.4 to 2.5 +/- 1.5 mg. The removal constant (K-A) from pool A (M
-A) did not change significantly with added dietary campestanol and sitosta
nol (K-A= - 0.040 +/- 0.005 v -0.037 +/- 0.007 d(-1)). The results demonstr
ate small campestanol plasma concentrations and body pools even when the ra
bbits consumed substantial amounts because (1) intestinal absorption was li
mited and (2) was further reduced by competing dietary sitostanol, and (3)
campestanol was removed rapidly from the body. Thus, campestanol, which sha
res the same basic structure and intestinal absorption pathway with cholest
erol, does not accumulate when fed, and may be incorporated into the diet t
o block cholesterol absorption. Copyright (C) 1999 by W.B. Saunders Company
.