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Journal of the American College of Nutrition, Vol. 22, No. 1, 80-87 (2003)
Published by the American College of Nutrition

Original Research

Postprandial Lipemia in Hypertension

Genovefa D. Kolovou, MD, Deliana Ch. Daskalova, MD, Stella A. Iraklianou, MD, Evdokia N. Adamopoulou, MD, Nektarios D. Pilatis, MD, Georgios C. Hatzigeorgiou, MD and Dennis V. Cokkinos, MD

Cardiology Department, Onassis Cardiac Surgery Center, Athens (G.D.K., D.Ch.D., E.N.A., N.D.P., G.C.H.), GREECE
3rd Medical Clinic, Tzanio Hospital, Piraeus (S.A.I.), GREECE

Address reprint requests to: Genovefa D. Kolovou, M.D., Onassis Cardiac Surgery Center, 356 Sygrou Ave., 176 74 Athens GREECE


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Objective: Many studies have shown that patients with coronary artery disease have an exaggerated rise and a delayed fall of plasma triglyceride (TG) concentration postprandially. We examined whether patients with essential hypertension have the same response to a fatty meal.

Methods: A fatty meal (350g per 2 m2 body surface with 83.5% fat) was given to 25 patients with essential hypertension (H) and to 25 normotensives (N). The two groups were matched for age, body mass index, lipid profile, basal glucose and insulin concentrations, and an index of homeostasis model of insulin resistance (HOMA-IR). A quantitative insulin sensitivity check index (QUICKI) was calculated. Blood samples were taken at 0, 4, 6, and 8 hours after the fatty meal. Lipid variables were measured in all samples. Blood glucose and insulin levels were measured in the fasting state.

Results: Total and high density lipoprotein cholesterol, apolipoprotein A1 and B, lipoprotein (a), HOMA-IR and QUICKI did not differ significantly over time between the groups. The plasma TG concentration (mg/dL) increased significantly after fat loading in H (from 118 ± 31 to 284 ± 137 at 4 hours, 327 ± 93 at 6 hours and 285 ± 71 at 8 hours) compared to N group (from 105 ± 29 to 150 ± 38 at 4 hours, 148 ± 40 at 6 hours and 115 ± 34 at 8 hours), p = 0.001, p < 0.001 and p < 0.001, respectively.

Conclusion: This study suggests that patients with hypertension have an exaggerated response and delayed clearance of plasma TG concentration after fat loading.

Key words: hypertension, hypertriglyceridemia, postprandial lipemia

Abbreviations: CAD = coronary artery disease • H = hypertensive patients • HOMA = index of homeostasis model of insulin resistance (HOMA-IR) [11] • N = normotensive subjects • TG = triglyceride


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Many individuals develop atherosclerotic disease despite normal fasting lipid values [1]. Numerous studies have consistently shown that, in the hours following a fatty meal, plasma triglyceride (TG) concentration is higher in patients with than in subjects without coronary artery disease (CAD) [2–3], and this is an independent risk factor for CAD [4]. The TG are not found in the atheromatous plaque [5,6]. However, TG rich lipoproteins are involved in many pathways leading to atherosclerosis: 1) they are carriers of cholesteryl ester to the vessel wall [6,7]; 2) they are toxic to the endothelial cells and induce endothelial dysfunction [8–11]; 3) the hypertriglyceridemic state is accompanied by small dense low density lipoproteins [12–15], which are more susceptible to oxidation and by low concentration of plasma high density lipoprotein cholesterol [15,16]. Beside the aforementioned functions, hypertriglyceridemia may be involved in events leading to thrombosis [17,18] and probably provoke arterial activation of nuclear factor-kappa B, which has been proposed as a key mediator of atherogenesis [19].

Despite the fact that hypertension is another strong risk factor for CAD, in almost all studies, lowering of the blood pressure in hypertensive patients has not produced the expected beneficial reduction in CAD risk [20]. This paradox may be explained by the multiple interrelated abnormalities in glucose and lipid metabolism, linking hypertension and the insulin resistance syndrome [21–25]. It is unknown whether hypertensive patients with normal values of fasting lipid profile, glucose and insulin, without obesity or any organ damage, have postprandial lipid abnormalities. Only a few data exist regarding the response of TG to a fatty meal in patients with essential hypertension whose baseline lipid values are within the normal range. We undertook this study to investigate this aspect of hypertension.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Study Population
The study population consisted of 50 Greek males. Smoking, heavy drinking, liver and renal diseases, obesity, diabetes mellitus, hypothyroidism, professional sports activity, total cholesterol minus high density lipoprotein cholesterol >200 mg/dL, TG >160 mg/dL and the use of any drug were exclusion criteria. No subject used a special hypolipidemic diet before entering this study. No subject was obese current to the study or in the past. The study subjects walked from 20 minutes to one hour two to three times a week, but nobody practiced vigorous sport activity. All persons gave informed consent. The study was approved by the Ethics Committee of the Onassis Cardiac Surgery Centre.

Subjects were divided into two groups:

  1. Hypertensive patients (H) consisted of 25 hypertensive patients with a negative CAD history and a negative maximal treadmill exercise test. They had a history of hypertension of at least three months’ duration and had several separate documented blood pressure measurements above 140/90 mm Hg. All a) had positive hypertensive response to treadmill exercise consisting of a rise of the systolic blood pressure >200 mm Hg and b) had mean blood pressure values >140/90 mm Hg during a working day using 24-hour Space Labs 90207 (SPACELABS MEDICAL, INC Redmond, WA) blood pressure monitoring; none c) had previously received antihypertensive treatment or were yet under a specific salt-restriction diet.
  2. Normotensive subjects (Controls, C) consisted of 25 individuals, medical personnel of the Onassis Cardiac Surgery Centre or their family members. They were free of any disease and had negative family histories for early atherosclerosis and hypertension. They had normal maximal treadmill exercise tests. All subjects had normal blood pressure (i.e. systolic blood pressure <130 mm Hg and diastolic blood pressure <85 mm Hg) at three measurements.

The C subjects were matched to H patients for body mass index, age, lipid variables and for index of homeostasis model of insulin resistance (HOMA-IR) [26].

Study Protocol
Patients were studied in the outpatient clinic between 7:00 am and 8:00 am after a 12-hour overnight fast. The fatty meal was consumed within 20 minutes, until 8:30 am, after which time the participants were instructed not to take anything orally except water for the subsequent eight hours. Blood samples were drawn at 8:00 am (before the meal), at 12:30 am (four hours after the meal), 2:30 pm (six hours after the meal) and at 4:30 pm (eight hours after the meal). In all four samples we measured total cholesterol, TG, high density lipoprotein cholesterol, apolipoproteins A1 and B, and lipoprotein (a).

Body mass index was calculated as weight divided by height expressed in kg/m2. Waist circumference, expressed in cm, was chosen as a measure of central adiposity as advised by the Executive Summary of The Third Report of The National Cholesterol Educational Program (NCEP), Adult Treatment Panel III [27] for evaluation of the patients, candidates for metabolic syndrome. To exclude insulin resistance syndrome, fasting blood glucose and insulin levels were measured and homeostasis model approximation (HOMA-IR) index [26] and quantitative insulin sensitivity check index (QUICKI) [28] were calculated. We assessed the whole-body insulin resistance with the following formulas: HOMA-IR = fast glucose x fast insulin/22,5 [26,29] and QUICKI parameter as 1/log insulin + log glucose in mg/dL [28].

Fat Loading.
The fatty meal was a slight modification of that introduced by Patsch et al. [1], consisting of 83.5% fat, 14.0% carbohydrates and 2.5% proteins and was given in a dose based on the patient’s body surface area (350 g to 2 m2 body surface, Table 1).


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  		Table 1. The Test Fatty Meal Content

 
Blood Chemistry.
Plasma total cholesterol and TG concentrations were measured enzymatically with a Dimension RxL instrument (AR Dade Behring, Newark, DE 19714, USA) with commercially available kits (Dade Behring). High density lipoprotein cholesterol was determined by measuring cholesterol concentration in the supernatant liquid after precipitation of the plasma with MgCl2 and dextran sulfate. Apolipoproteins A1 and B were measured by nephelometry (Nephelometer: BN-100, Behring, Germany). Blood glucose was measured by the hexokinase method with a Dade Behring reagent on a Dimension (Dade Behring) instrument and the blood insulin with the IMX ABBOTT Diagnostics instrument. All samples were analyzed within 24 hours.

Statistical Analysis and Presentation of Results
All variables were tested for normality using the Shapiro-Wilk W test, since the size of each sample was smaller than 50 subjects. The significance of the differences between the two groups was determined with a) independent samples t test (Student’s t test) for the variables following normal distribution, b) Mann-Whitney U Test with downward adjustment of the level of significance for the variables found to deviate significantly from normal distribution. All values are expressed as mean ± SD. A p-value of less than 0.05 was considered significant. Correlations between continuous variables were tested with Pearson’s method for normally distributed variables and with Spearman’s method for not-normally distributed variables. Repeated measures ANOVA was used to test the differences in the three TG measurements (4, 6 and 8 hours) between H and C subjects after the fatty meal.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 
All participants tolerated the fatty meal well. The amount of fatty meal ingested by the H patients was 333 ± 15 g and by the C subjects 341 ± 23 g.

Baseline Characteristics
Baseline characteristics are shown in Table 2. No significant differences were noted between the two groups except for the blood pressure.


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  		Table 2. Baseline Characteristics of the Study-Subjects

 
Postprandial Changes
Plasma total and high density lipoprotein cholesterol, apolipoprotein A1 and B, and lipoprotein (a) did not change significantly after fat loading in any one of the groups.

A) TG changes at 4 hours: The plasma TG concentration (in mg/dL) was increased significantly more in H (from 118 ± 31 to 284 ± 137) compared to C group (from 105 ± 29 to 150 ± 38), p = 0.001, Mann-Whitney U test (Fig. 1).



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  		Fig. 1. Plasma triglyceride concentrations in hypertensives and normals at baseline, 4 hours, 6 hours and 8 hours after a fat-rich meal. H = hypertensive patients, N = Normal subjects, TG0 = triglyceride concentrations (TG) at baseline, TG4 = TG four hours after a fat rich meal, TG6 = TG six hours after a fat rich meal, TG8 = TG eight hours after a fat rich meal.

 
B) TG changes at 6 hours: Plasma TG concentration (in mg/dL) was increased significantly more in H (from 118 ± 31 to 327 ± 93) compared to C group (from 105 ± 29 to 148 ± 40), p < 0.001, Mann-Whitney U test (Fig. 1).

C) TG changes at 8 hours: Plasma TG concentration (in mg/dL) was significantly higher in H (from 118 ± 31 to 285 ± 71) compared to C group (from 105 ± 29 to 115 ± 34), p < 0.001, Student’s t test (Fig. 1).

Repeated measures ANOVA gave a p-value <0.001 for the difference between H and C subjects with respect to TG level response to a fatty meal at 4, 6 and 8 hours. This indicates that at 4, 6 and 8 hours after the fat load there was a significantly higher level of TG in H than in C group. The absolute increase in the TG concentration (in mg/dL) from the baseline values in H group vs. C group was as follows: 148 ± 103 vs. 45 ± 28 (p < 0.001) at 4 hours, 209 ± 76 vs. 43 ± 36 (p < 0.001) at 6 hours and 167 ± 60 vs. 10 ± 38 (p < 0.001) at 8 hours.

Postprandial TG Response Differences between Groups
Apart from the differences between mean values, only three hypertensive patients had postprandial TG concentrations equal or lower than 219 mg/dL, which was the highest value (at 4 hours) attained by the normotensive controls. Furthermore, at 6 and 8 hours postprandially no overlap of TG values was observed.

Correlation between Highest Postprandial TG Concentrations and BMI, Waist Circumference, HOMA-IR and QUICKI Parameters.
The correlations between BMI, waist circumference and HOMA-IR were evaluated carried out by Pearson’s method. For correlation with QUICKI parameter we used Spearman’s method. In H group BMI correlates significantly and positively with the TG concentrations postprandially (r = 0.515, p = 0.01 at 6 hours and r = 0.405, p = 0.049 at 8 hours), whereas in C group such correlation did not appear (r = 0.202 at 6 hours and r = 0.063 at 8 hours).

However, no correlation was found between the highest postprandial TG concentration and waist circumference, HOMA-IR and QUICKI parameters either in H patients and in C subjects. Because the normal values for HOMA-IR are still under discussion and ranged from 2.0 [30] to 2.5 [31], we subdivided our study population to those with HOMA-IR <2.0 (n = 11 in H group and n = 10 in C group) and to those with HOMA-IR <2.0 (n = 14 in H group and n = 15 in C group) and recalculated their correlation with the highest postprandial TG concentration. No correlation was found in all subgroups.


   DISCUSSION
 
In the present study we investigated the effect of a fatty meal on plasma TG concentration in middle-aged untreated hypertensive men. Middle-aged men with hypertension already have two risk factors for CAD, and an abnormal response of plasma TG concentrations to a fatty meal would be an additional one. The relationship between postprandial hyperlipidemia and CAD was described by many research groups [2–4, 32–35]. In all of these studies the patients with clinically documented atherosclerosis were found to have an elevated postprandial TG response to a fatty meal. Essential hypertension is a classic and strong risk factor for CAD. This urged us to search for any additional abnormalities which would aggravate the prognosis of H patients.

It has been reported that H patients have higher baseline blood lipid concentrations than normotensive individuals. In the Oslo study [36], it was shown that middle-aged men with diastolic blood pressure above 110 mm Hg had average plasma cholesterol concentrations greater by 27 mg/dL compared to those with a diastolic blood pressure below 70 mm Hg. In the Göteborg primary prevention study [37], even when blood pressure was reduced, the H patients who went on to have a myocardial infarction had higher mean plasma cholesterol concentrations than those who remained event-free. Sharret et al. [38] and Karpe et al. [39] was reported that elevated postprandial TG are an independent risk factor for carotid intimal thickening. Considering that carotid intimal thickening is also seen in hypertension [40–42], a common denominator between intimal thickening, hypertension, and lipid handling abnormalities can be envisaged. Recently Bokemark et al. [43] were found that only triglycerides and pulse pressure contributed independently to the variability in the common carotid intima-media thickness.

Hypertension is classically associated with insulin resistance, defined as an inappropriately high insulin concentration relative to glycaemia. Studies have demonstrated that hyperinsulinemia can induce an overproduction of TG-rich lipoproteins in the liver by increasing the availability of free fatty acids, which are the most important precursors of de novo TG synthesis. To assess insulin sensitivity, DeFronzo et al. [44] introduced the technique "euglycaemic hyperinsulinemic glucose clamp" which, however, cannot be applied to large samples. Thus, the measurement of circulating concentrations of radioimmunoassayable insulin and glucose, either fasting or following a glucose load, is the most widely used method. Temple et al. [45] have demonstrated the lack of specificity of currently available radioimmunoassay techniques for measuring circulating insulin concentrations, mainly due to cross-reactivity of the antibody with proinsulin and various proinsulin-split products. We did not study this aspect. In our study, fasting glucose and insulin concentrations were normal and similar in our two groups. For more precise screening for eventual insulin resistance we used HOMA-IR and QUICKI methods. The HOMA-IR is a classical method of approximate estimation of insulin resistance, however has excellent correlation with more formal and cumbersome techniques [28,46,47] and is currently accepted as a good marker for insulin resistance [29]. Even more, the HOMA-IR was found to correlate significantly with euglycemic hyperinsulinemic clamp exactly among hypertensive and normotensive patients [48]. In our present work the HOMA-IR index was similar in both groups, in the normal range [31], and did not correlate to postprandial TG concentrations. The new QUICKI method [28] is a simple and accurate way for insulin resistance diagnostics in common clinical and epidemiological practice [49] and was found to highly correlate with fasting insulin and HOMA-IR [50]. Besides the fact that the QUICKI, as well the other two surrogate methods for estimating insulin resistance (fasting insulin and HOMA-IR), correlated relatively weakly with the direct assessment of insulin-mediated glucose disposal (r = 0.60–0.64) [50], this index had lower dispersion variances and a higher discrimination capacity [49]. None of our study subjects have had more than two of the risk determinants of the metabolic syndrome according to the last NCEP [27]. Our results could not have been influenced by antihypertensive treatment since none of our H or C individuals was on treatment.

We reported an abnormal plasma TG response to a fatty meal in hypertensive patients with normal fasting lipids and lipoprotein levels who do not fulfill the diagnostic criteria for the metabolic syndrome [51]. Iaina et al. [52] found, in a group of untreated nondiabetic essential hypertensive patients with no fasting lipid abnormalities and matched control normotensive individuals, that hypertensives after a fatty meal with vitamin A as a marker had higher chylomicron fraction concentration curves (AUC 17.469 ± 2.553 µg/L/hour vs. AUC 13.208 ± 1.245 µ/L/hour in controls, p < 0.001). However, the study group was smaller (14 hypertensives and 15 controls), and many of the hypertensives had borderline or abnormal glucose tolerance tests. No methods to evaluate insulin resistance were used. In our present study we demonstrate that the postprandial lipid abnormalities are independent of eventual insulin resistance syndrome, as was defined in the last (NCEP), Adult Treatment Panel III [27], and accompanied systemic hypertension from its early stage.

Definite normal ranges for TG response to a fatty meal test are still not established. In the present study the highest TG level postprandially in controls was 219 mg/dL. Eighty-eight per cent of H patients had postprandially TG levels >219 mg/dL. However, H patients differed clearly from the C group. Firstly, C subjects achieved peak TG concentration at 4 hours after the fat load, while H patients had delayed peak (at 6 hours). Secondly, in all H patients TG values at 6 hours postprandially were higher than in any of the C individuals, including the C peak levels. Furthermore, despite the fact that in the present study the H were slightly thinner, a significant positive correlation between BMI and maximal TG concentration postprandially was found in H but not in C. This might suggest that hypertensives must be advised more strongly to keep body weight in the normal ranges than normotensives.

One limitation of this study is that our work does not address the underlying biological mechanism for the abnormal triglycerides response to a fatty meal among middle-aged essential hypertensive men without clinically apparent metabolic syndrome. Postprandial hypertriglyceridemia is probably a consequence of competition between chylomicrons and very low density lipoprotein cholesterol for the lipoprotein lipase. Classically, chylomicron clearance occurs in two sequential steps: 1) TG hydrolysis by lipoprotein lipase, 2) uptake of the remnant by the liver. Delay in the second step leads to accumulation of remnants in plasma and is generally thought to represent the atherogenic risk of postprandial hypertriglyceridemia. A chylomicron particle must gain access to an unoccupied lipoprotein lipase molecule on the capillary surface of adipose tissue or cardiac and skeletal muscle. This means that the rate of TG clearance is the result of many variables [53–56] such as the size of the respective capillary beds, the amount of active lipoprotein lipase and the number of the very low density lipoprotein particles competing with chylomicrons. We can speculate that some of the above described abnormalities could be the mechanism of the postprandial lipemia in hypertensive patients demonstrated in this study.

Another hypothesis may be that the arterial hypertension and the postprandial TG increase seem to appear first in the earliest stage of the metabolic syndrome before it is possible to detect the insulin resistance with the commonly used methods [26,28]. Clinical insulin resistance is usually defined by reduced insulin-mediated uptake of glucose in skeletal muscle [57]. New data suggest that the endothelial cell itself can be insulin-resistant [57] and could reduce blood flow and increase peripheral vascular resistance with resultant clinically detectable hypertension. In humans, insulin-induced vasodilatation is mediated by nitric oxide release [58,59]. On the other hand, essential hypertension is characterised by a defect of endothelial nitric oxide synthesis [60]. A single gene defect [61] or the polymorphism of endothelial nitric oxide synthase gene [62] could be the missing link between hypertension and metabolic disorders, including postprandial hypertriglyceridemia.

Beck-Nielsen [57] does not exclude the possibility that TG and fatty free acids can induce insulin resistance in cellular level. It still being discussed whether TG increase postprandially can provoke clinically undetectable cellular insulin resistance in patients with uncomplicated essential hypertension.

Enhanced activity of the sympathetic nervous system may be present from the earliest stage of essential hypertension [63], when the postprandial hypertriglyceridemia was detected in our H patients and, at least theoretically, a relation between the two could not be excluded.

Postprandial hypertriglyceridemia is not a uniform abnormality. Its pathophysiologic cause is not yet known. It is possible that the response to a fatty meal is gene dependent. It has been reported that a number of gene loci, such as these of apolipoprotein E, lipoprotein lipase, apolipoprotein CIII, apolipoprotein A1, apolipoprotein A4, cholesterol ester transfer protein and of FABP2, are related to the fat load response [64–66]. But this gene polymorphism dependence remains controversial, and it is more likely that the postprandial lipemia is a polygenic phenomenon, although the phenotype of the postprandial lipemia is probably one. This concept allowed us to study only the phenotypical manifestation of the postprandial lipemia which would have immediate clinical implications. Our aim was to evaluate whether the hypertensive patients had postprandial lipid abnormalities. We did not investigate either the exact pathophysiological mechanism responsible for postprandial lipemia or its genetic basis.


   CONCLUSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
ACKNOWLEDGMENTS
 REFERENCES
 
Our findings show that the untreated middle-aged men with uncomplicated essential hypertension have an abnormal response to a fatty meal—increased TG levels and delayed TG clearance. We can speculate that this fact may be an additional reason for the higher incidence of CAD among these patients and may lead to a new concept for the treatment of the hypertension, having as target the possible postprandial TG abnormalities, along with the usual antihypertensive medications.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
REFERENCES
 
We are grateful to Alexandra Valaora, dietician, for expertly managing the patients during the meal.

Received February 22, 2002. Accepted August 23, 2002.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 CONCLUSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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