![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Service de Diabétologie, Nutrition et Maladies Métaboliques & Centre d'Investigation Clinique/INSERM, CHU de Nancy, Hôpital Jeanne d'Arc, 54201 Toul cedex, B.P. 303, France;
*
Laboratoire de Biochimie, Hôpital Broussais AP-HP, 75014 Paris et Faculté de Pharmacie Paris XI, 92296 Chatenay-Malabry, France;
Clinique Médicale B U 62, CHU de Reims, 51092 Reims, France; and
**
Clinique Médicale et Endocrinologique, CHU de Dijon, 21000 Dijon, France
2To whom correspondence should be addressed.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
KEY WORDS: • postprandial lipemia • circadian variations • oral fat load test • retinyl palmitate • humans
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
, Zilversmit 1979
). Many studies
comparing patients with coronary artery disease and controls have
demonstrated differences in postprandial triglyceride after an oral fat
load test (OFLT) (Nikkila et al. 1994
) and that the
postprandial triglyceride concentration is an independent predictor of
coronary artery disease in multivariate analysis (Patsch et al. 1992
). A delayed clearance of retinyl palmitate, used to study
the metabolism of TRL of intestinal origin, discriminates between
patients with coronary artery disease and controls (Groot et al. 1991
, Simpson et al. 1990
), even after
adjustment for fasting triglyceride or HDL cholesterol in
normolipidemic men (Weintraub et al. 1996
).
The fat tolerance tests as currently performed differ from one study to
another. There is no consensus about the time at which the study should
begin; postprandial tests usually begin in the morning (Durlach et al. 1996
, Patsch et al. 1992
), but they can
also start in the afternoon (Chen et al. 1992
), or even
at night (Zampelas et al. 1994
). Bed rest is also
required (Aldred et al. 1994
), and the energy and fat
load are high, making the study of postprandial lipemia using the OFLT
a very unphysiologic situation. A nocturnal OFLT could be a suitable
way to improve the conditions of the fat load because bed rest and
fasting after the fat load are easier during the night time. A
nocturnal fat test allows postprandial blood samples to be taken for
10 h without any need to alter the subjects' normal meal pattern.
This study was therefore conducted to compare the lipid responses of normolipidemic young men after OFLT given at 2200 h (nocturnal) and at 0700 h (diurnal). The changes in the concentrations of retinyl palmitate and triglyceride were monitored for 10 h in both tests.
|
SUBJECTS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Nine healthy male Caucasian volunteers were recruited from the local
University and studied in the Nancy Clinical Research Center
(INSERM-CHU). They satisfied the following criteria: 1)
normal body mass index (20–25 kg/m2); 2)
stable body weight (<2% change in the last 3 mo); 3)
age 20–30 y; 4) no symptoms of illness or ongoing
medication; 5) no family history of premature coronary
disease (before age 60 y); 6) moderate alcohol
intake (<20 g/d); and 7) never smoked. They were all
normal on physical examination, had normal glucose tolerance assessed
by oral glucose tolerance test and normal blood chemistry profiles
including the following: creatinine, sodium, potassium, chloride, total
protein, total and direct bilirubin, and activities of aspartate or
alanine aminotransferase and 
-glutamyl transferase. Their fasting
lipid profiles were normal, i.e., LDL cholesterol <3.9 mmol/L, HDL
cholesterol >0.90 mmol/L and triglyceride <1.25 mmol/L. The
participants maintained their usual physical activities and diet
throughout the study. This project was approved by the Ethics committee
of the Nancy University Hospital and informed written consent was
obtained from all subjects.
Study protocol.
All subjects underwent two consecutive OFLT. Each subject served as his
own control. The time between tests was 14 ± 1 d. Nocturnal
and diurnal tests were performed in a random order. Five subjects did
the first test starting in the morning and four in the late evening
(Fig. 1
). Subjects attended our Clinical Research Center at least 12 h
before the beginning of the OFLT. They were instructed to refrain from
strenuous exercise and any alcohol for 3 d before the OFLT.
|
)
(2890 kJ with 31% fat, 19% protein and 50% carbohydrate) at
2030 h on the day before the diurnal fat load. They fasted for
10 h, until 0700 h, at which time the diurnal oral fat load
was given. Subjects were given the same calibrated meal at 1130 h
on the morning before taking the nocturnal fat load. They fasted for
10 h, until 2200 h, when the nocturnal fat load was given. Dietary assessments.
A 5-d dietary record, including a weekend and three weekdays, was examined to determine the usual energy intake and the proportion of fats, carbohydrates and proteins of the subjects before each test. Subjects were asked to keep accurate dietary records, including food items and beverages consumed and accurate estimates of portion sizes. Food models and standard utensils were used to demonstrate portion sizes (Replica Food Limited, Hobson House, London, U.K.). Food and energy intakes were calculated using a computerized nutrient database (GENI; Micro 6, Nancy, France).
Oral fat load test (OFLT).
The fat load was 180 g of a manufactured emulsified blended meal composed of 3.5% dried skimmed milk, 19.25% butter, 23.75% peanut oil, 22% chocolate, 30.25% water, 0.75% gelatin, 0.25% sorbic acid and 0.25% potassium sorbide (Laboratoire Pierre Fabre Santé, Castres, France). Its energy content was 3720 kJ (85% fat, 13% carbohydrates, 2% protein), with 35 g saturated fatty acid, 30 g monounsaturated fatty acid, 15 g polyunsaturated fatty acid and 88 mg cholesterol. The fatty acid composition of the OFLT was determined by gas chromatography. The OFLT contained 1.25% of the total fatty acids as 10:0, 1.5% as 12:0, 3.1% as 14:0, 20.3% as 16:0, 12.3% as 18:0, 43.7% as 18:1, 13.3% as 18:2 and 1.08% as 20:0. The fat load was ingested in 15 min with 200 mL water; 100,000 IU retinyl ester (Avibon 50,000 IU; Theraplix-Rhone Poulenc Rorer, Paris, France) was added to the fat load to label intestinally derived lipoparticles. No further food or drink was allowed during the study. The participants remained supine and slept normally throughout the nocturnal test. They were instructed to remain in bed, supine, for the diurnal test.
Sleep quality.
Sleep quality was assessed in the morning immediately after taking the last sample of the nocturnal OFLT by using an analog visual scale. One hundred percent represented an ideal night and 0% a sleepless night.
Biochemical measurements.
A 21-gauge venous canula was placed in an antecubital vein. Blood
samples were collected 30, 20 and 10 min before the ingestion of the
fat load to determine plasma insulin and glucose concentrations. The
means of the three values were taken as basal values. Blood samples
were then taken immediately before the fat load and 2, 3, 4, 5, 6, 8
and 10 h after (T0, T2, T3, T4, T5, T6, T8 and T10). Plasma
glucose and insulin concentrations were measured at T0 and T2.
Apolipoprotein (apo) AI and apo B, plasma total LDL and HDL
cholesterol, HDL2 and HDL3 cholesterol
concentrations were determined at T0. For all samples from T0 to T10,
15 mL blood was drawn into vacutainer collection tubes to determine
triglyceride and retinyl palmitate in the plasma and in the chylomicron
and nonchylomicron fractions. All blood samples were immediately
centrifuged at 1000 x g for 15 min at 4°C.
Phenylmethylsulfonyl fluoride (10 mmol/L in isopropanol) and aprotinin
(Trasylol, Bayer Pharma, Puteaux, France) were immediately added to the
plasma to final concentrations of 10 and 28 µmol/L,
respectively (Karpe et al. 1995
). The plasma was then
frozen at -20°C until final analysis. Plasma glucose was determined
soon after centrifugation. The chylomicron fraction (supernatant) was
isolated by ultracentrifugation for 30 min at 120,000 x
g in a Beckman XL-80 ultracentrifuge, rotor
Ti-SW 41(Palo Alto, CA). The infranatant was collected and named
the nonchylomicron fraction; it contained triglyceride-rich
lipoproteins (chylomicron remnants, VLDL and VLDL remnants). Mean
recovery (± SD) of triglyceride was 98 ± 3%.
Total cholesterol and triglyceride were determined enzymatically
(bioMérieux, Marcy l'Etoile, France). HDL cholesterol was
assessed by phosphotungstic acid precipitation, and LDL cholesterol was
calculated according to the Friedewald formula (Friedewald et al. 1972
). HDL2 and HDL3 cholesterol
concentrations were determined by a direct electrophoretic method in a
discontinuous gradient gel (Atger et al. 1991
). Apo AI
and apo B were determined by immunonephelometry with commercial kits
(Beckman, Gagny, France).
Retinyl palmitate was measured by reverse-phase HPLC (System Gold,
Beckman), according to De Ruyter and De Leenheer (1978)
.
The detection limit was 0.018 mg/L. Plasma glucose was determined by
enzymatic colorimetric method (PAP 250, bioMérieux). Total plasma
insulin concentration was determined by immunoenzymatic assay (Insulin
IMX, Abbott Laboratories, Tokyo, Japan). Cross reactivity with
proinsulin was <0.05%.
The apo E genotypes were obtained by Hha I restriction
after polymerase chain reaction (Hixson and Vernier 1990
).
Statistical analysis.
Data are expressed as means ± SD, n
= 9. When the distribution of a variable was not normal, as
assessed by Skewness and Kurtosis tests, data were log-transformed,
and statistical analysis was done on the log-transformed data.
Areas under the OFLT time-dependent concentration curves (area
under curve, AUC) were calculated by the trapezoidal rule
(Matthews et al. 1990
). Incremental AUC (AUCi) was
evaluated after subtracting the initial individual values (T0) for
triglyceride from all respective postprandial measurements, yielding
the net postprandial change.
The relative postprandial change was determined for plasma triglyceride after subtracting the initial value for triglyceride from all respective postprandial measurements and subsequently dividing it by the initial value for triglyceride, i.e., [(Tx - T0)/T0]. This method allows the time at which the triglyceride concentration returned to baseline to be more clearly identified and takes into account differences in the initial value of triglyceride between each test.
The period was defined as the order of the test (first administered diurnally or nocturnally). ANOVA was used for a crossover study with period, postprandial times, and interaction factors. Two-way repeated-measures ANOVA was used to assess the effect of postprandial times on postprandial triglyceride and retinyl palmitate concentrations. When ANOVA was significant, or when variables were measured only once, means were compared by Student's paired t test. The association between two continuous variables was determined by the linear regression coefficient. The level of significance was P < 0.05. Statview IV.5 software (Abacus Concepts, Berkeley, CA) was used for all calculations.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Table 1
summarizes the clinical and laboratory characteristics of the subjects.
The OFLT was well tolerated. No subject suffered from nausea or
reported any adverse reactions.
|
Mean sleep quality was 59.3 ± 14.6% (range: 43–88%). Sleep quality was significantly better if the subjects had done the diurnal OFLT first (68.4 ± 13.5) than if the nocturnal OFLT was done first (48 ± 4.4%, P < 0.03).
Conventional postprandial lipid parameters.
The plasma triglyceride peak concentrations for the diurnal and
nocturnal tests did not differ (Table 2
). The total AUC and AUCi for plasma triglyceride from the two tests
were similar. The triglyceride peak values and the AUC of triglyceride
in the chylomicron and nonchylomicron fractions were not significantly
different in the two tests.
|
Kinetics of the postprandial lipemic response.
The triglycerides reached peak values at different times in the diurnal
and nocturnal lipemic responses (P < 0.05) (Table 2
, Fig. 2A
). The nocturnal peak occurred significantly later than the diurnal peak
in seven of the nine subjects. Two-way repeated-measures ANOVA
showed a significant effect of the interaction between the time of the
fat load test administration and postprandial times on triglyceride
concentrations (f = 5.03, P < 0.0001),
indicating that the curves for plasma triglyceride concentrations after
each test were significantly different.
|
A). The plasma
triglyceride concentration had returned to its initial value at T8; it
continued to decrease between T8 and T10 in the diurnal test, but
remained above baseline at T10 in the nocturnal test (Fig. 2
B).
Two-way repeated-measures ANOVA showed a significant effect of the
interaction between the time of the fat load test administration and
postprandial times on triglyceride concentrations in the chylomicron
and nonchylomicron fractions (f = 3.24, P
< 0.004 and f = 8.83, P < 0.0001, respectively), indicating that the changes in the triglyceride
concentrations after the two tests differed (Fig. 3
). The kinetic responses after OFLT for lipid subfractions were similar
to those for total plasma triglycerides. Triglyceride peak times in the
chylomicron and nonchylomicron fractions were similar to one another
and were synchronous with total plasma triglyceride peak times, i.e.,
5.8 ± 1.7 h after nocturnal OFLT, and 4.3 ± 1.2 h
after diurnal OFLT (P < 0.05).
|
The total plasma retinyl palmitate peak time tended to be later after a
nocturnal OFLT than after a diurnal OFLT (Table 2
, Fig. 4
). Two-way repeated-measures ANOVA showed no significant effect of
the interaction between the time of the fat load test administration
and postprandial times on plasma retinyl palmitate concentrations
(f = 1.92, P = 0.073). The nocturnal
peak time occurred later than the diurnal peak time in only four of the
nine subjects. The retinyl palmitate concentrations at T8 and T10
tended to be higher after nocturnal OFLT than after diurnal OFLT (0.86
± 0.51 vs. 0.49 ± 0.42 mg/L, P = 0.08 and
0.55 ± 0.39 vs. 0.29 ± 0.28 mg/L, P = 0.06,
respectively).
|
The plasma insulin concentrations at T0 for the diurnal (41 ± 18 pmol/L) and nocturnal (25 ± 9 pmoI/L) OFLT were not different (P > 0.05). The diurnal and nocturnal insulin concentrations at T2 also did not differ (76 ± 28 vs. 85 ± 31 pmol/L).
A postprandial test model.
We have tried to predict the postprandial AUC (pAUC) from three triglyceride determinations instead of the eight measurements carried out during these tests to reduce the number of blood samples taken and the number of biochemical determinations done in routine clinical practice. Two models were developed. The three triglyceride determinations used for the first were as follows: triglycerides at T0, at individual peak concentrations and at T10. The second model used the triglyceride values at T0, at average peak time (T4 for diurnal and T6 for nocturnal tests) and at T10. The pAUC was divided by the total AUC measured by the trapezoidal rule, and data for the two tests were compared.
The first model gave a diurnal pAUC that was correlated with total diurnal AUC (r = 0.92, P < 0.001). The nocturnal pAUC was also positively and significantly correlated with total nocturnal AUC (r = 0.99, P < 0.0001). The ratios of pAUC/total AUC were 110.3 ± 11.7% for diurnal OFLT and 107 ± 6.4% for nocturnal OFLT. The CV of this ratio was 10.6% after the diurnal test and 6% after the nocturnal test.
The second model gave a diurnal pAUC that was correlated with the
diurnal total AUC (r = 0.90, P < 0.001). The nocturnal pAUC was also significantly correlated with the
nocturnal total AUC (r = 0.98, P < 0.0001) (Fig. 5
). The ratios of pAUC/total AUC were 97.1 ± 14.8% for the diurnal
OFLT and 95.0 ± 9.1% for the nocturnal OFLT. The CV of this
ratio was 15.3% after the diurnal test and 9.6% after the nocturnal
test.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
). However, the usual OFLT is a
very unphysiologic test, with bed rest for a large part of the day
(Aldred et al. 1994
), no food intake after the fat load
and a fat meal that provides a very unusual energy and fat intake in
the early morning (often >100 g fat) (Patsch et al. 1983
, Weintraub et al. 1996
). We have therefore
looked for a more convenient oral fat load test. Bed rest, drinking
restrictions and fasting after the fat load are more readily obtained
during the night, and energy and fat intakes are higher at dinner than
at breakfast or lunch (Fricker et al. 1990
,
Winkler et al. 1995
). The fat load (80 g) used in our
OFLT was close to the usual fat intake of the subjects during dinner
(75 g on average). Finally, the use of a nocturnal fat test allowed a
10-h postprandial blood sampling, without any need to alter the
subjects' normal meal patterns.
The subjects were instructed to continue their usual activities before
the test meal to minimize potential confounding factors because
exercise alters lipid metabolism (Aldred et al. 1994
,
Foger and Patsch 1995
). Subjects refrained from
strenuous exercise during the 3 d before the tests to limit the
influence of acute exercise. No alcohol was allowed in the 3 d
preceding each test because alcohol also alters lipid metabolism
(Hartung et al. 1993
, Pownal, 1994
). The
body weight of all subjects was constant throughout the study. A
constant energy, total and saturated fat, carbohydrate and protein
intake was ensured, and the food intake before each test was identical.
The time between tests was 14 ± 1 d; this was similar to the
time in a previous study that indicated good reproducibility between
two consecutive oral fat loads (Brown et al. 1992
).
No subject suffered from nausea or reported any adverse reactions. Tolerance of the test and the quality of the participants' sleep were assessed subjectively. Sleep during the nocturnal test was not too different from normal (59.3 ± 14.6%). The subjects also reported that the oral fat load was more easily ingested at 2200 h than at 0700 h. They considered the nocturnal fat load to be more convenient because they could not drink or eat and had to remain supine during both tests. This was harder during the diurnal test. Thus, the nocturnal OFLT appeared to be well tolerated.
The lipid response curves obtained during the diurnal OFLT are in
agreement with those of previous studies on postprandial responses. The
mean plasma triglyceride peak after an oral fat load occurred 4 h
later (Karpe et al. 1995
, Lewis et al. 1990 and 1991
). The mean plasma triglyceride peak times obtained in
several studies is one of the three triglyceride diurnal determinations
(T4) that we used in our second postprandial model. The synchronous
nature of the triglyceride peak times in the plasma, chylomicron and
nonchylomicron fractions has also been reported (Schrezenmeir et al. 1992
). The times of the triglyceride peaks in the
chylomicron and nonchylomicron fractions may be similar because the
triglyceride-rich lipoproteins derived from the liver
(nonchylomicron fraction) account for a large part of the postprandial
lipemia responses (Karpe et al. 1995
). Others have
demonstrated that 80% of the increase in postprandial
triglyceride-rich lipoprotein particles is accounted for by VLDL
(Schneeman et al. 1993
). The mean plasma peak of retinyl
palmitate occurred 4.5 h after the oral fat load in our study, in
agreement with the findings of others (Cortner et al. 1987
, Uiterwaal et al. 1994
), although some have
reported a later peak time (Heller et al. 1993
,
Patsch et al. 1992
).
The postprandial retinyl palmitate and triglyceride concentrations for
the diurnal and nocturnal fat loads were not different, taking into
account the usual postprandial variables, i.e., peak values, AUC and
AUCi. The triglycerides and retinyl palmitate in the plasma and in the
chylomicron and nonchylomicron subfractions were similar. The
triglyceride peak concentrations in the two tests were also
significantly correlated. These results are in agreement with those of
Romon et al. (1997)
, who found no difference in the AUC
of triglyceride, VLDL-triglyceride and serum cholesterol for the
diurnal and nocturnal tests. However, the sleep-wake rhythm was
deliberately disturbed in this study, and the test meals were given at
different times, with the nocturnal test beginning at 0100 h.
Finally, the plasma triglyceride peak times were not different
(Romon et al. 1997
).
The nocturnal lipid response occurred significantly more slowly, with
the plasma and chylomicron and nonchylomicron triglyceride peak times
occurring significantly later. The initial triglyceride concentrations
(T2) were higher in the diurnal test, whereas the late triglyceride
concentrations (T8, T10) were lower than in the nocturnal
concentrations. The nocturnal curve appeared to be shifted to the right
and the triglyceride concentrations remained above the baseline T0
concentrations at T10. Although they did not compare diurnal and
nocturnal lipid responses, Zampelas et al. (1994)
were
the first to perform a nocturnal fat load test and to show that the
postprandial triglyceride curves reached their maxima 5–7 h after the
fat load. Our results are in keeping with those of Hampton et al. (1996)
, who simulated nocturnal OFLT by shifting the
biological clocks of nine subjects. The test meals were given at 0100
and 2100 h. The nocturnal triglyceride values were delayed much
like those reported here (Hampton et al. 1996
).
The delayed lipemic response reported here and by others may be due to
slower gastric emptying at night (Goo et al. 1987
).
Direct assessment of gastric emptying in diurnal and nocturnal OFLT may
be required to confirm this. The slower removal of TRL during the night
may also shift the triglyceride nocturnal curve to the right, perhaps
because of a nocturnal decrease in glucose tolerance (Van Cauter et al. 1989
). The triglyceride peak was delayed after a diurnal
fat tolerance test in the more glucose-intolerant patients, i.e.,
those patients with diabetes and hypertriglyceridemia had a later
triglyceride peak than the nondiabetic controls (Lewis et al. 1991
).
We believe this is the first time that nocturnal retinyl palmitate
postprandial metabolism has been determined. We found no difference
between the diurnal and nocturnal retinyl palmitate concentrations, for
the AUC or the peak concentrations, in the plasma or in the chylomicron
and nonchylomicron fractions. In addition, there was no significant
difference between the times of the diurnal and nocturnal plasma
retinyl palmitate peaks. Slow gastric emptying decreases intraluminal
lipolysis (Maes et al. 1996
), and gastric emptying is
significantly less rapid in the evening than in the morning in humans
(Goo et al. 1987
). Because retinyl palmitate metabolism
is especially linked to pancreatitic cholesterolesterase and a specific
brush border hydrolase, plasma retinyl palmitate could be less
influenced by the rate of intraluminal lipolysis than plasma
triglycerides (Rigtrup and Ong 1992
). In addition, in
our study four of the nine healthy subjects had a second nocturnal
plasma retinyl palmitate peak, whereas only one of nine had a
second plasma triglyceride peak. A second postprandial retinyl
palmitate peak has been reported in several studies (Cohn et al. 1989
). These second peaks occur 8–10 h after the meal and may
reflect delayed gastric emptying (Bergeron and Havel 1997
). In our study, the difference between diurnal and
nocturnal second plasma retinyl palmitate peaks tended to be
significant (P < 0.05; data not shown).
The AUC is the most frequently used index for evaluating postprandial
lipemia (Durlach et al. 1996
, Patsch et al. 1992
, Simpson et al. 1990
) and is a discriminant
marker between controls and patients with altered postprandial TRL
removal (Karpe and Hamsten 1995
, Miesenbock and Patsch 1992
). The two models developed to reduce the numbers of
blood samples taken and processed are both satisfactory; the pAUC was
correlated with the AUC, particularly during the nocturnal test. The
first model cannot be used in routine clinical practice because the
individual triglyceride peak concentrations vary. The second model
appears to be more suitable because the pAUC may be calculated from
three lipid determinations, regardless of the individual peak values
(T6 for nocturnal test). We also checked this second model of pAUC on a
population with various stages of insulin resistance and obesity (17
obese patients and 33 healthy controls). Using the same postprandial
test model during the diurnal period, we showed that the pAUC is
correlated with the AUC measured by the trapezoidal rule (unpublished
data). In addition, the level of significance between obese subjects
and controls was higher with pAUC than with AUC, confirming the
discriminant power of the predicted postprandial AUC with three
triglyceride determinations instead of the eight or more usually used
(unpublished data). Finally, the smaller CV for the nocturnal lipid
response, when expressed as the pAUC/total AUC ratio, also indicates
that the nocturnal test is more suitable for epidemiologic studies than
are the diurnal fat tolerance tests.
However, our study was conducted in a small group of normolipidemic healthy subjects. We do not yet know whether this model can be applied to other populations who were eligible for oral fat load tests. Further studies are required to assess its reliability in larger studies over a wide range of circumstances. Nevertheless, nocturnal OFLT appears to be well tolerated and convenient for use in healthy normocholesterolemic individuals. The number of lipid determinations may be reduced to three to make this test suitable for use in larger studies. However, these data must be confirmed, particularly in patients affected by abnormal triglyceride removal.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
3 Abbreviations used: apo, apolipoprotein; AUC,
area under the curve; AUCi, incremental AUC; OFLT, oral fat tolerance
test; pAUC, predicted area under the curve; RP, retinyl palmitate; TRL,
triglyceride-rich lipoproteins.
Manuscript received December 18, 1998. Initial review completed January 25, 1999. Revision accepted May 24, 1999.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Aldred H. E., Perry I. C., Hardman A. E. The effect of a single bout of brisk walking on postprandial lipemia in normolipidemic young adults. Metabolism 1994;43:836-841[Medline]
2.
Atger V., Malon D., Bertière M. C., N'Diaye F., Girard-Globa A. Cholesterol distribution between high-density-subfractions HDL2 and HDL3 determined in serum by discontinuous gradient gel electrophoresis. Clin. Chem. 1991;37:1149-1152
3. Bergeron N., Havel R. J. Assessment of postprandial lipemia: nutritional influences. Curr. Opin. Lipidol. 1997;8:43-52[Medline]
4.
Brown S. A., Chambless L. E., Sharrett A. R., Gotto A. J., Patsch W. Postprandial lipemia: reliability in an epidemiologic field study. Am. J. Epidemiol. 1992;136:538-545
5. Chen Y. D., Skowronski R., Coulston A. M., Pietarinen J., Hollenbeck C. B., Reaven G. M. Effect of acute variations in dietary fat and carbohydrate intake on retinyl ester content of intestinally derived lipoproteins. J. Clin. Endocrinol. Metab. 1992;74:28-32[Abstract]
6. Cohn J. S., McNamora J. R., Krasinski S. D., Russell R. M., Schaefer E. J. Role of triglyceride-rich lipoprotein from the liver and intestine in the etiology of postprandial peaks in plasma triglyceride concentration. Metabolism 1989;38:484-490[Medline]
7. Cortner J. A., Coates P. M., Le N. A., Cryer D. R., Ragni M. C., Faulkner A., Langer T. Kinetics of chylomicron remnant clearance in normal and in hyperlipoproteinemic subjects. J. Lipid Res. 1987;28:195-206[Abstract]
8.
De Ruyter M.G., M & De Leenheer A. P. Simultaneous determination of retinol and retinyl esters in serum or plasma by reversed-phase high performance liquid chromatography. Clin. Chem. 1978;24:1920-1924
9. Durlach V., Attia N., Zahouani A., Leutenegger M., Girard-Globa A. Postprandial cholesteryl ester transfer and high density lipoprotein composition in normotriglyceridemic non-insulin-dependent diabetic patients. Atherosclerosis 1996;120:155-165[Medline]
10. Foger B., Patsch J. R. Exercise and postprandial lipaemia. J. Cardiovasc. Risk 1995;2:316-322[Medline]
11. Fricker J., Giroux S., Fumeron F., Apfelbaum M. Circadian rhythm of energy intake and corpulence status in adults. Int. J. Obes. 1990;14:387-393[Medline]
12. Friedewald W. T., Levy R. I., Frederickson J. Estimation of the concentration of low-density cholesterol in plasma without the use of the preparative ultra-centrifuge. Clin. Chem. 1972;18:499-502[Abstract]
13. Goo R. H., Moore J. G., Greenberg E., Alazraki N. Circadian variation in gastric emptying of meals in humans. Gastroenterology 1987;93:515-518[Medline]
14.
Groot P.H.E, Van Stiphout W.A.H.J., Krauss X. H., Jansen H., Van Tol A., Van Ramshorst E., Chin-On S., Hofman A., Cresswell S. R., Havekes L. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arterioscler. Thromb. 1991;11:653-662
15. Grundy S. M. National Cholesterol Education Program: second report of the expert panel on detection, evaluation, and treatment of high blood cholesterol in adults. Circulation 1994;89:1329-1445
16. Hampton S. M., Morgan L. M., Lawrence N., Anastasiadou T., Norris F., Deacon S., Ribeiro D., Arendt J. Postprandial hormone and metabolic responses in simulated shift work. J. Endocrinol. Investig. 1996;151:259-267
17. Hartung G. H., Lawrence S. J., Reeves R. S., Foreyt J. P. Effect of alcohol and exercise on postprandial lipemia and triglyceride clearance in men. Atherosclerosis 1993;100:33-40[Medline]
18. Heller F. R., Vandenplas C., Desager J. P., Harvengt C. The vitamin A fat-loading test in young normolipidemic subjects. Clin. Chim. Acta 1993;219:167-176[Medline]
19. Hixson J., Vernier D. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with Hha I. J. Lipid Res. 1990;31:545-548[Abstract]
20.
Karpe F., Bell M., Björkegren J., Hamsten A. Quantification of postprandial triglyceride-rich lipoproteins in healthy men by retinyl ester labeling and simultaneous measurement of apolipoproteins B-48 and B-100. Arterioscler. Thromb. Vasc. Biol. 1995;15:199-207
21. Karpe F., Hamsten A. Postprandial lipoprotein metabolism and atherosclerosis. Curr. Opin. Lipidol. 1995;6:123-129[Medline]
22.
Lewis G. F., O'Meara N. M., Soltys P. A., Blackman J. D., Iverius P. H., Druetzler A. F., Getz G. S., Polonsky K. S. Postprandial lipoprotein metabolism in normal and obese subjects: comparison after the vitamin A fat-loading test. J. Clin. Endocrinol. Metab. 1990;71:1041-1050
23.
Lewis G. F., O'Meara N. M., Soltys P. A., Blackman J. D., Iverius P. H., Pugh W. L., Getz G. S., Polonsky K. S. Fasting hypertriglyceridemia in noninsulin-dependent diabetes mellitus is an important predictor of postprandial lipid and lipoprotein abnormalities. J. Clin. Endocrinol. Metab. 1991;72:934-944
24.
Maes B. D., Ghoos Y. F., Geypens B. J., Hiele M. I., Rutgeerts P. J. Relation between gastric emptying rate and rate of intraluminal lipolysis. Gut 1996;38:23-27
25. Matthews J.N.S, Altman D. G., Campbell M. J., Royton P. Analysis of serial measurements in medical research. Br. Med. J. 1990;300:230-235
26. Miesenböck G., Patsch J. R. Postprandial hyperlipidemia: the search for the atherogenic lipoprotein. Curr. Opin. Lipidol. 1992;3:196-201
27. Nikkila M., Solakivi T., Lehtimaki T., Koivula T., Laippala P., Astrom B. Postprandial plasma lipoprotein changes in relation to apolipoprotein E phenotypes and low density lipoprotein size in men with and without coronary artery disease. Atherosclerosis 1994;106:149-157[Medline]
28.
Patsch J. R., Karlin J. B., Scott L. W., Smith L. C., Gotto A. M. Inverse relationship between blood levels of high density lipoprotein subfraction 2 and magnitude of postprandial lipemia. Proc. Natl. Acad. Sci. U.S.A. 1983;80:1449-1453
29.
Patsch J. R., Miesenböck G., Hopferwieser T., Mühlberger V., Knapp E., Dunn J. K., Gotto A. M., Patsch W. Relation of triglyceride metabolism and coronary artery disease. Arterioscler. Thromb. 1992;12:1336-1345
30. Pownal H. J. Dietary ethanol is associated with reduced lipolysis of intestinally derived lipoproteins. J. Lipid Res. 1994;35:2105-2113[Abstract]
31. Rigtrup K. M., Ong D. E. A retinyl ester hydrolase activity intrinsic to the brush border membrane of rat small intestine. Biochemistry 1992;31:2920-2926[Medline]
32.
Romon M., Le Fur C., Lebel P., Edmé J. L., Fruchart J. C., Dallongeville J. Circadian variation of postprandial lipemia. Am. J. Clin. Nutr. 1997;65:934-940
33.
Schneeman B. O., Kotite L., Todd K. M., Havel R. J. Relationship between the responses of triglyceride-rich lipoprotein in blood plasma containing apolipoproteins B-48 and B-100 to fat-containing meal in normolipidemic humans. Proc. Natl. Acad. Sci. U.S.A. 1993;90:2069-2073
34. Schrezenmeir J., Weber P., Probst R., Biesalski H. K., Luley C., Prellwiz W., Krause U., Beyer J. Postprandial pattern of triglyceride-rich lipoprotein in normal-weight humans after an oral lipid load: exaggerated triglycerides and altered insulin response in some subjects. Ann. Nutr. Metab. 1992;34:186-196
35. Simpson H. S., Williamson C. M., Olivecrona T., Pringle S., Maclean J., Lorimer A. R., Bonnefous F., Bogaievsky Y., Packard C. J., Shepherd J. Postprandial lipemia, fenofibrate and coronary artery disease. Atherosclerosis 1990;85:193-202[Medline]
36.
Uiterwaal C.S.P.M., Grobbee D. E., Witteman J.C.M, Van Stiphout W.A.H.J., Krauss X. H., Havekes L. M., De Brujin A. M., Van Tol A., Hofman A. Postprandial triglyceride response in young adult men and familial risk for coronary atherosclerosis. Ann. Intern. Med. 1994;121:576-583
37.
Van Cauter E., Desir D., Decoster C., Fery F., Balasse E. G. Nocturnal decrease in glucose tolerance during constant glucose infusion. J. Clin. Endocrinol. Metab. 1989;69:604-611
38.
Weintraub M. S., Grosskopf I., Rassin T., Miller H., Charach G., Rotmensch H. H., Liron M., Rubinstein A., Iaina A. Clearance of chylomicron remnants in normolipidaemic patients with coronary artery disease: case control study over three years. Br. Med. J. 1996;312:935-939
39. Winkler G., Doring A., Keil U. Mealtime patterns in a southern German population. Results from the WHO MONICA 1984/1985 Augsburg nutritional survey project. Z. Emahrungswiss. 1995;34:2-9
40. Zampelas A., Peel A. S., Gould B. J., Wright J., Williams C. M. Polyunsaturated fatty acids of the n-6 and n-3 series: effects on postprandial lipid and apolipoprotein levels in healthy men. Eur. J. Clin. Nutr. 1994;48:842-848[Medline]
41.
Zilversmit D. B. Atherogenesis: a postprandial phenomenon. Circulation 1979;60:473-485
This article has been cited by other articles:
|
|
 |
|
  A. J. Hooper, K. Robertson, P. H. R. Barrett, K. G. Parhofer, F. M. van Bockxmeer, and J. R. Burnett Postprandial Lipoprotein Metabolism in Familial Hypobetalipoproteinemia J. Clin. Endocrinol. Metab., April 1, 2007; 92(4): 1474 - 1478. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. D. Mattes Oral Fat Exposure Increases the First Phase Triacylglycerol Concentration Due to Release of Stored Lipid in Humans J. Nutr., December 1, 2002; 132(12): 3656 - 3662. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
