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Department of Human Nutrition, Kansas State University, Manhattan, KS 66506
2To whom correspondence should be addressed. E-mail: koo{at}humec.ksu.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-tocopherol, and
100 PC in 24 mL PBS, pH 6.6]. The PC in the lipid emulsion was egg PC
(EPC), hydrogenated egg PC (HPC), or soy PC (SPC). The EPC in the lipid
emulsion markedly lowered the lymphatic absorption of
14C-CH (24.7 ± 2.5% dose) compared with SPC (34.9
± 1.2%) and a lipid emulsion containing no PC (NPC) (30.8
± 2.0%). The HPC further lowered the absorption of
14C-CH to 21.1 ± 1.4% dose. The outputs of
phospolipid were unaffected by the source of PC infused (EPC, 32.2
± 1.7; HPC, 31.8 ± 1.6; and SPC, 32.9 ± 1.8
µmol/8 h). Compared with NPC (595.0 ± 59.5
µmol), the total output of fatty acids over 8 h
was increased significantly by SPC (685.4 ± 55.8
µmol), but decreased by HPC (467.7 ± 28.4
µmol). The total lymphatic output of oleic acid
(18:1), the major fatty acid infused in the form of triolein, did not
differ among the NPC (448.0 ± 58.2 µmol/8 h),
SPC (457.9 ± 52.3 µmol/8 h) and EPC (412.9
± 20.8 µmol/8 h) groups, but was significantly
lower in the HPC group (262.0 ± 24.1 µmol/8 h).
The findings provide the first evidence that EPC markedly lowers the
lymphatic absorption of cholesterol under in vivo conditions. The
inhibitory effect of EPC appears to be due to the higher degree of
saturation of its acyl groups relative to SPC, suggesting that the
intestinal absorption of egg cholesterol may be reduced by the presence
of PC in egg yolk.
KEY WORDS: • phosphatidylcholine • cholesterol • intestinal absorption • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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, isolated brush border
membranes (2)
, everted intestinal sacs (3
,4)
and perfused small intestine (5)
.
Recent studies showed that pancreatic phospholipase
A2 (pPLA2), when added to
micellar solutions, abolished the PC-induced inhibition of
cholesterol uptake in Caco-2 cells in vitro (1
,6)
. Another
study with intestinal cells demonstrated that addition of
pPLA2 in a lipid emulsion facilitated the
hydrolysis of triacylglycerol (TG) and, subsequently, increased
cholesterol uptake (7)
. These observations are in line
with the earlier findings that diether PC inhibits cholesterol uptake
from the intestinal lumen because the ether PC is resistant to
hydrolysis by pPLA2 (8
9
10)
.
However, the mechanism underlying the inhibitory effect of PC on
cholesterol absorption is yet to be elucidated. Furthermore, it is not
known whether a normal range of dietary PC intake interferes with
cholesterol absorption under in vivo conditions. Although PC is
hydrolyzed efficiently by pPLA2
(11)
, evidence shows that PC containing unsaturated fatty
acids (FA) are hydrolyzed more readily by the enzyme than those with
saturated FA (12)
. Therefore, saturation of the acyl
groups may slow the rate of PC hydrolysis by
pPLA2 and, hence, the intestinal absorption of
cholesterol. In this study using conscious rats with lymph cannula, we
examined whether egg and soy PC differing in saturation of the acyl
groups differentially affect intestinal cholesterol absorption.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Male Sprague-Dawley rats (n = 20; Harlan
Sprague Dawley, Indianapolis, IN) weighing 228.3 ± 9.8 g
were placed individually in plastic cages with stainless steel wire
bottoms in a windowless room maintained at 22–25°C and subjected to
a daily 12-h light:dark cycle with the light period from 1530 to
0330 h throughout the study. Upon arrival, the rats were fed a
diet (Table 1
) formulated by Dyets (Bethlehem, PA) according to the AIN-93G
recommendations (13)
. The mineral mix was modified
according to the recommendations of Reeves (14)
to adjust
the mineral contents with the use of egg white as the protein source.
All rats were housed in an animal care facility in the Department of
Human Nutrition, Kansas State University, accredited by the American
Association for the Accreditation of Laboratory Animal Care. They were
given free access to deionized water via a stainless steel watering
system. Animals were maintained in accordance with the policies and
guidelines for animal care and use procedures of the Kansas State
University Institutional Animal Care and Use Committee.
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At 5 wk, rats were deprived of food for 16 h. The mesenteric lymph
duct was cannulated as described previously (15
,16)
. After
the rat was anesthetized with halothane, an abdominal incision was made
along the midline. The major intestinal lymph duct was cannulated with
polyethylene tubing (SV.31 tubing, i.d., 0.50 mm; o.d., 0.80 mm; Dural
Plastics, Auburn, Australia). An indwelling infusion catheter (Silastic
medical grade tubing, i.d., 1.0 mm; o.d., 2.1 mm; Dow Corning, Midland,
MI) was introduced via the gastric fundus into the upper duodenum and
secured by a purse-string suture (4–0 Silk; Ethicon, Somerville,
NJ). After the abdominal incision was closed, the rats were placed in
restraining cages in a heated chamber (30°C) for postoperative
recovery for 22–24 h. During the recovery period, rats were infused
via the infusion catheter with PBS (in mmol/L: 277 glucose, 6.75
Na2HPO4, 16.5 NaH2PO4,
115 NaCl and 5 KCl, pH 6.6) at 3.0 mL/h by a syringe pump (Harvard
Apparatus, Model 935, South Natick, MA).
Measurement of the lymphatic absorption of 14C-cholesterol.
After postoperative recovery, each rat was infused via the duodenal
catheter at 3 mL/h for 8 h with a lipid emulsion consisting of
451.8 µmol triolein, 27.8 kBq
[4-14C]-cholesterol (14C-CH; specific
activity, 1.9 GBq/mmol, DuPont NEN, Boston, MA), 20.7
µmol CH, 3.6 µmol -tocopherol, and
396.0 µmol sodium taurocholate with 100
µmol PC or without PC in 24 mL of PBS (6.8 mmol/L
Na2HPO4, 16.5 mmol/L
NaH2PO4, 115 mmol/L NaCl and 5 mmol/L KCl, pH
6.6). To prepare the lipid emulsion, the lipid mixture and PBS were
placed in an amber bottle and sonicated under gentle N2
stream and subdued light for 50 min by using a
microprocessor-controlled ultrasonicator equipped with a microtip
(XL-2020 Ultrasonic Liquid Processor;Misonix,Farmingdale,NY). The PC
included in the lipid emulsion was soy PC (SPC; >99%), egg yolk PC
(EPC; >99%), or hydrogenated egg yolk PC (HPC; >99%). All PC were
purchased from Avanti Polar Lipids (Alabaster, AL). The fatty acid
compositions of these phospholipids are shown in Table 2
. During lipid infusion, lymph samples were collected hourly under
subdued light in preweighed ice-cold centrifuge tubes containing 4
mg Na2-EDTA and 30 µg
n-propyl gallate (Sigma Chemical, St. Louis, MO). The hourly
lymph samples (100 µL) were mixed with scintillation
liquid (ScintiVerse; Fisher Scientific, Fair Lawn, NJ) and counted to
determine 14C-radioactivity appearing in the
lymph (Beckman LS-6500; Beckman Instruments, Fullerton, CA).
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. An aliquot (100
µL) of lymph was added dropwise into a centrifuge tube
containing 1 mL acetone/ethanol (1:1, v/v); then 20 µL of
10% glacial acetic acid and 0.5 mL of 0.5% freshly made digitonin
solution (100 mg digitonin in 20 mL 50% ethanol) were added. The tube
was capped, mixed well and allowed to stand at room temperature for
1 h. After centrifugation at 1500 x g at 4°C
for 20 min, the supernatant (EC fraction) was removed carefully with a
Pasteur pipette. To the precipitate (FC fraction), 1.0 mL of
acetone/ether (1:2, v/v) was added. The mixture was centrifuged for 30
min, and the supernatant was removed. The precipitate was redissolved
in 100 µL of ethanol, mixed with 10 mL scintillation
cocktail (ScintiVerse; Fisher Scientific), and counted to determine
14C-radioactivity in the FC fraction (Beckman
LS-6500; Beckman Instruments, Fullerton, CA). The
14C-radioactivity in the EC fraction was
calculated by total 14C-radioactivity in the
unfractionated lymph minus
14C-radioactivity in the FC fraction. Phospholipid and FA analysis.
Total lipids from 100 µL lymph were extracted
(18)
by 2 mL of chloroform/methanol mixture (2:1, v/v)
containing 10 mg of BHT/300 mL. An internal standard (19:0) was added
during lipid extraction. Lymph phospholipid (PL) was measured by the
method of Raheja et al. (19)
, as modified previously
(15)
. For FA analysis, the lipids were hydrolyzed with
methanolic NaOH, and FA were saponified and methylated simultaneously
with BF3-methanol, as described by Slover and Lanza
(20)
. The fatty acid methyl esters were analyzed by
capillary gas chromatography (Hewlett-Packard, Model 6890, Palo Alto,
CA) using a HP-INNOWax cross-linked polyethylene glycol phase
capillary column (30 m, i.d. 0.25 mm; Hewlett-Packard, Wilmington,
DE).
Statistics.
All statistical analyses were performed using PC SAS (SAS Institute, Cary, NC). Repeated-measures ANOVA followed by the least significant difference test were conducted. Differences were considered significant at P < 0.05. Values are means ± SD.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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In response to lipid infusion, lymph flow increased rapidly in all
groups and peaked at 4–5 h. The rates of lymph flow did not differ
among the four groups. The hourly rates of lymph flow were 2.6 mL/h in
rats infused with a lipid emulsion containing no PC (NPC), 2.2 mL/h in
SPC, 2.3 mL/h in EPC and 2.6 mL/h in the HPC group. The total lymph
volume for 8 h was slightly lower in the SPC group than in the NPC
and HPC groups, but did not differ from that in EPC rats (Table 3
).
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The total absorption of 14C-CH over 8 h was
significantly lower in the EPC group than in the NPC control (Table 3)
.
When HPC was infused, the lymphatic absorption of
14C-CH was further decreased. The absorption of
14C-CH for the 8-h period was significantly
higher in SPC rats than in all other groups. The cumulative absorption
of 14C-CH, as determined at hourly intervals, was
significantly lower in EPC and HPC than in SPC rats beginning at 2 h and thereafter (Table 4
). The absorption of 14C-CH was consistently
higher in SPC than in NPC rats. The average rate of
14C-CH absorption in SPC, EPC and HPC rats was
4.4 ± 0.1, 3.1 ± 0.3 and 2.6 ± 0.2% dose/h,
respectively, with significant differences among the three groups. The
absorption rate in NPC rats (3.8 ± 0.3% dose/h) was
significantly lower than in SPC but higher than in EPC and HPC groups.
The 14C-radioactivities in the EC fractions, as
expressed in % total, did not differ among the PC-infused groups.
Significantly more 14C-radioactivity was
distributed in the EC fraction in NPC rats compared with other groups
except at 2 h (Fig. 1
).
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No significant differences were observed in hourly lymphatic PL output
among PC-infused groups. However, PL output in the NPC rats began
to decline at 5 h and remained significantly lower thereafter than
in the PC-infused groups (Fig. 2
). The total amount of PL released over 8 h was less in the NPC
rats than in all other groups (Table 3)
.
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Table 5
summarizes the lymphatic outputs of individual FA and total FA during
lipid infusion for 8 h. Compared with the NPC rats, the total FA
output was significantly higher in SPC rats, but lower in HPC rats. NPC
and EPC groups did not differ in total FA output. The cumulative
lymphatic output of 18:1, which was the major FA infused in the form of
triolein, did not differ among the NPC, SPC and EPC groups, but was
significantly lower in the HPC group. The lymphatic 18:1 output rates
were 56.0 ± 7.3 in NPC, 57.2 ± 6.5 in SPC, 51.6 ± 2.6
in EPC and 32.8 ± 3.0 µmol/h in HPC rats.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Studies have documented that, under physiologic conditions, dietary or
biliary PC serves as the major source of PC for formation of the
surface PC of chylomicrons, facilitating intestinal absorption of fat
(21
,22)
. In view of the overall stimulatory effect of PC
on fat absorption, the precise mechanism underlying the PC-mediated
inhibition of cholesterol absorption remains unclear. Evidence from an
earlier in vitro study (10)
suggested that PC increases
the size of bile salt micelles in the intestinal lumen, thus slowing
their passage across the unstirred water layer to the absorptive cells.
As the concentration of PC increases in a micellar matrix, the apparent
molecular weight of a mixed micelle increases and the rate of micellar
diffusion through the unstirred layer decreases, slowing cholesterol
uptake by enterocytes (4
,23
,24)
. In contrast,
lysophophatidylcholine (lysoPC) micelles are smaller than PC micelles,
resulting in higher cholesterol uptake from the lysoPC micelles
(4
,25)
.
In keeping with the above-cited observations, a study by
Borgström (24)
using porcine
pPLA2 in vitro showed that EPC inhibited
hydrolysis of the core TG in a lipid emulsion and that a limited
initial hydrolysis of the surface PC by pPLA2
facilitated the binding of pancreatic lipase and colipase to the
substrate, accelerating TG hydrolysis. A recent study using IEC-6
intestinal cells (7)
demonstrated that when the molar
ratio of PC to TG in a lipid emulsion is >0.3,
pPLA2-mediated hydrolysis of the surface PC is
necessary for the effective hydrolysis of TG in the core by pancreatic
lipase/colipase and for stimulation of cholesterol uptake by the
intestinal cells. Other studies using Caco-2 cells also showed that
addition of PLA2 or substitution of lysoPC for PC
in mixed micelles reverses the PC-induced inhibition of cholesterol
uptake (1
,6)
. The above-cited evidence indicates that
PC, whether in mixed micelles or in lipid emulsions, interferes with
the intestinal uptake of cholesterol by altering the rates of micellar
formation and diffusion and/or impeding the hydrolysis of TG and
subsequent uptake of cholesterol. However, as discussed above,
information available thus far has been obtained from in vitro studies
using intestinal segments (4
,23
,25)
or intestinal cell
lines (1
,6
,7)
.
This study is the first to compare the effects of egg and soy PC on the
intestinal absorption of cholesterol in conscious rats with lymph
cannula. An important new finding is that under in vivo conditions, not
all PC inhibit intestinal cholesterol absorption and that the
PC-induced inhibition of cholesterol absorption depends on the
degree of saturation of the acyl moiety. Among the PC used here, the
degree of FA saturation increased in the order of SPC < EPC
< HPC. The majority (77%) of the FA in SPC were unsaturated,
with 18:2 accounting for 61% of the total FA content. In contrast, EPC
contains mostly saturated (45%) and monounsaturated FA (18:1, 32%),
and 18:2 represents <18% of the total FA content of EPC. Hydrogenated
egg PC (HPC) is composed entirely of saturated FA, of which 16:0 and
18:0 account for 
91%. The lymphatic absorption of cholesterol
decreased with increasing saturation of the PC infused. Also, the total
lymphatic outputs of FA decreased significantly in the same order. The
highest level of lymphatic FA output was observed with SPC. The FA
outputs with EPC and HPC infusion were reduced to 89 and 68%,
respectively, of the output level observed with SPC infusion. The
lymphatic output of 18:1, which was the major FA infused in the form of
triolein in the lipid emulsion, tended to decrease with increasing
saturation of the PC. The 18:1 output was lowest when HPC was infused.
Thus, our data indicate that a PC with saturated acyl groups can
decrease the lymphatic absorption of cholesterol as well as the
lymphatic output of FA as incorporated into lymph lipids. Similarly,
the significant increases in lymphatic cholesterol and FA output
produced by SPC over the control levels (no PC infusion) may be
explained by the differences in FA makeup between soy and biliary PC.
In the rats not infused with PC, the bile was the sole source of
luminally available PC. Biliary PC of rats contains predominantly
saturated FA (16:0 and 18:0) at sn-1, which results in
marked inhibition of pPLA2 activity
(12)
.
The lower outputs of FA with relatively more saturated PC may be
attributable to slower hydrolysis of the core TG in the lipid emulsions
coated with saturated PC. Because saturated PC are poor substrates for
pPLA2 and not hydrolyzed readily
(12)
, their presence would hinder pancreatic lipase from
accessing the core TG of the emulsion particle and thereby slowing the
formation and diffusion of micelles and uptake of lipids by the
enterocyte. This view is supported by the earlier findings that the
presence of PC in lipid emulsions slows TG hydrolysis by pancreatic
lipase even in the presence of bile salts and colipase
(24
,26
,27)
. These observations also are consistent with
the recent in vitro finding that initial hydrolysis of PC by
pPLA2 is required for hydrolysis of TG in a lipid
emulsion and for stimulation of cholesterol uptake by intestinal cells
(7)
.
The possibility exists, however, that factors other than the degree of
saturation of the acyl moiety of PC may influence cholesterol
absorption. The PC used here differed in their acyl chain length. For
example, SPC was devoid of longer-chain saturated FA such as 20:0
and 22:0, whereas HPC contained small amounts of these FA. It is
unclear whether these FA are liberated during PC hydrolysis in amounts
sufficient to hinder cholesterol absorption. Our data on lymph FA
output showed that 20:0 and 22:0 were not detectable in the mesenteric
lymph collected, suggesting that their release and absorption from the
PC may be minimal. A question also arises concerning whether the
stimulatory effect of SPC on cholesterol absorption and total FA output
might be associated in part with enrichment of luminal lipids with 18:2
derived from the hydrolysis of SPC infused or secreted through the
enterohepatic recirculation during lipid infusion. It is unlikely,
however, that infusion of SPC contributed to luminal 18:2 enrichment
via the enterohepatic pathway because little enterohepatic recycling or
reutilization of luminal (biliary) PC or its FA is shown to occur
during fat absorption (28
,29)
. Furthermore, a recent study
(30)
showed that a diet enriched with 18:2 does not
increase cholesterol absorption compared with one enriched with 18:1 or
16:0, whereas an equivalent amount of dietary 18:0 significantly lowers
cholesterol absorption.
It is of interest to note that despite the expected difference in the
rate of PC hydrolysis, the lymphatic outputs of PL were unaffected by
the PC infused. This finding is consistent with the observations by
others that exogenous PL added to the normal biliary supply does not
markedly influence the lymphatic output of PL (31
,32)
.
Previous studies (33
34
35)
also have shown that, once taken
up by the enterocyte, excess lysoPC is hydrolyzed to FA and
glycerol-3-phosphocholine (GPC). Much of the FA is incorporated into TG
within the enterocyte, and GPC is transported via the portal vein into
the liver for further metabolism. Thus, evidence suggests that the
enterocyte is capable of regulating the intracellular processing of PC
and the amount of PC secreted into the lymph depending on the cellular
demand for PC during chylomicron synthesis (31
32
33
34
35)
.
In this study, we found that the percentage of distribution of labeled
cholesterol in the lymphatic EC fraction was significantly lower when
PC was infused, regardless of its source. However, no significant
differences were noted in the lymphatic outputs of labeled EC among the
PC-infused groups, indicating that luminal PC, not the degree of PC
saturation, reduces cholesterol esterification and that the inhibition
of cholesterol absorption by PC is not attributable directly to their
inhibitory effects on cholesterol esterification within the enterocyte.
Evidence from in vitro studies using Caco-2 cells indicates that the
presence of PC in the incubation medium decreases the esterification
and secretion of cholesterol from intestinal cells independent of TG
secretion (1
,36)
. However, a direct effect of PC itself on
cholesterol esterification is unlikely because the uptake of intact PC
by the enterocyte is negligible. The effect of PC probably is mediated
via lysoPC generated by hydrolysis of PC by pPLA2
or brush border membrane PLA2 (37)
.
LysoPC, as readily taken up by the enterocyte, has been shown to
decrease cholesterol esterification in Caco-2 cells, possibly by
inhibiting acyl-CoA:cholesterol acyltransferase activity
(38)
.
Our observation of the pronounced decrease in cholesterol absorption
produced by EPC is of particular interest in view of the high
concentration of PC in egg yolk. A fresh egg yolk weighing 20 g
(from a 70-g whole egg) contains 1.7 mmol (1.3 g) PC and 0.9 mmol
(260 mg) cholesterol (39)
. At present, no data are
available to show that the PC in egg yolk lowers the intestinal
absorption of cholesterol in humans consuming eggs. Evidence from
numerous human studies shows that despite the high content of
cholesterol in egg yolk, consumption of one or two eggs per day has
little effect on blood cholesterol levels and coronary heart disease
risk (40
41
42)
. Our data show that EPC is more effective
than SPC in lowering cholesterol absorption. Previously, Beil and
Grundy (43)
observed that intraduodenal infusion of 30 g/d
of soy lecithin in human patients markedly decreased cholesterol
absorption. This effect may have been associated with infusion of an
unusually large amount of PC into short (50- and 100-cm) bowel
segments, considering that the normal range of daily PC intake is
estimated to be 4–8 g for normal human adults (11)
. In
the present study, the amount of PC infused was 100 µmol
of PC via a lipid emulsion. This amount of PC was estimated to be 0.75
mg/(kJ · d) on the basis of the rat’s average daily food intake of
20 g (297 kJ), which is equivalent to a daily intake of 7.9 g
PC for a human consuming 10,450 kJ (2500 kcal)/d. Thus, whether SPC
consumed in moderate amounts would lower cholesterol absorption in
normal humans remains to be determined. Studies have shown that daily
intakes of 10–20 g soy lecithin in hyperlipidemic humans have little
influence on blood cholesterol levels and lipoprotein profiles
(44
,45)
, despite the observation of a hypocholesterolemic
effect of SPC in animals (46
47
48
49)
.
In summary, the results of this study provide evidence that under in vivo conditions, EPC lowers the intestinal absorption of cholesterol. Our data here show that EPC is more effective than SPC in lowering cholesterol absorption. This effect of EPC appears to be associated with the higher degree of saturation of its fatty acyl groups. Further studies are warranted to determine whether the high concentration of PC in egg yolk reduces the intestinal absorption of egg cholesterol in humans.
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FOOTNOTES |
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3 Abbreviations used: 14C-CH,
14C-cholesterol; EC, esterified cholesterol; EPC, egg PC;
FA, fatty acid; FC, free cholesterol; GPC, glycerol-3-phosphocholine;
HPC, hydrogenated egg PC; lysoPC, lysophosphatidylcholine; NPC, lipid
emulsion containing no PC; PC, phosphatidylcholine; PL, phospholipid;
pPLA2; pancreatic phospholipase A2; SPC, soy
PC; TG, triacylglycerol.
Manuscript received January 10, 2001. Initial review completed March 28, 2001. Revision accepted June 5, 2001.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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