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Mathematical modeling of cholesterol homeostasis 57

of cholesterol in hepatic blood plasma and in the peripheral blood plasma as
equal to m 1 (t 0 )¼1235mg and m 2 (t 0 )¼4465mg, respectively. We assumed
that at t 0 ¼0, a meal containing 500mg of cholesterol was consumed.
Because cholesterol is insoluble in water it has to be contained in food
together with fats. Therefore, such a meal results in the release of bile from
the gallbladder, which carries some amount of cholesterol with an amplitude
of M out ¼9.6mgmin 1 calculated for m bile ¼4000mg (Mok et al., 1974) and
time of release of bile t 1 ¼50min (Di Ciaula et al., 2012) (Eq. 15). As a result,
we observed a decrease in the total concentration of cholesterol (c 2 ) and an
appropriate increase in the kinetics of cholesterol biosynthesis. The choles-
terol released into the duodenum returns with bile to the liver through the
portal vein between t 2 ¼70min and t 3 ¼300min ( Johnson, 2013). The
1
amplitude of this process (M in ¼1.96mgmin ) was calculated based on
Eq. (12) assuming a loss of 6% (Guyton and Hall, 2016). The expected result
is an increase in the level of cholesterol during this time. Finally, the cho-
lesterol from food is absorbed between 400 and 530min after the consump-
tion of a meal with an amplitude of M diet ¼2.3mgmin 1 (Eq. 16). For this to
happen, the cholesterol must first enter the small intestine, from where the
majority of it is absorbed in the form of chylomicrons, which are gradually
transformed into the remnants and move into the circulatory system. The
expected result of dietary intake of cholesterol is an increase in its concen-
tration (c 2 ) and the accompanying reduction in the rate of de novo cholesterol
synthesis. The profile obtained for the total change in the concentration of
cholesterol in the peripheral blood plasma is physiologically justified. In an
experiment conducted on 26 volunteers who received a fatty meal, contain-
ing 1.0g of fat/kg body weight and 7.0mg/kg of cholesterol, an analogous
profile was obtained (after adding up the results according to the Fridewald’s
rule (Friedewald et al., 1972)Tc¼LDL+HDL+0.2TG, where Tc—is total
cholesterol, LDL and HDL—are the lipoprotein fractions, and TG—
triglyceride) (Cohn et al., 1988).
The maintenance of normal physiological levels of blood cholesterol is
recognized as an important factor in preventing the development of CVDs.
Preventing adverse changes means focusing on a healthy and active lifestyle.
The simple two-compartment model of cholesterol homeostasis presented
in this study makes it easier to understand the mechanisms that lead to an
increase in the level of blood cholesterol. This model shows that there is
an increase in the concentration of cholesterol with age when the tissue
demand decreases (by lowering the value of m tis parameter). Disorders in
any of the multistage process of cholesterol exchange between the two com-
partments can also lead to adverse changes in cholesterol metabolism. This