In the present study it was observed that after the lipid overload test, the behavior of lipoproteins was similar in the adolescents with excess weight and eutrophic adolescents. In agreement with our findings, Moreno et al.
] evaluated postprandial lipemia in adolescents (12 obese and 12 non-obese, aged 11.0 to 13.8 years) and also found no significant differences between the groups. Tiret et al.
] in the European Atherosclerosis Research Study (EARS) compared the postprandial TG response of offspring whose father had suffered a myocardial infarction before the age of 55 years with controls in different populations in Europe. They found no differences between cases and controls in the postprandial TG response. It seems that the exaggerated postprandial lipemia in children and adolescents only concerns those with underlying lipid metabolic disorders.
The post-prandial lipemia curve is evaluated by the magnitude of the response to the stimulus (duration and/or extension) which corresponds to the time it takes to return to the baseline TG value, and by the amplitude that corresponds to the time at which the maximum value found occurs after lipid overload [15
]. In normolipemic individuals at fasting, an increase is shown in the concentrations of lipoproteins rich in TG, in the form of an ascendant curve 2 h after eating, with its peak occurring at approximately the 4th
hour, and with return to baseline values close to the 6th
]. However, in individuals with dyslipidemia, the peak of lipoproteins rich in TG is observed later, between the 4th
hours, with the return to baseline levels taking longer (after 8 hours) [17
]. The same phenomenon occurs in individuals with insulin resistance [15
]. In the present study, it was observed that adolescents with excess weight, irrespective of the presence of fasting hypertriglyceridemia, presented the TG peak in the fourth hour, and the eutrophic adolescents, independent of the fasting state, had an earlier TG peak in the second hour. However, considering the increase in TG concentrations (Δ T4- T0), no difference was noted between the two groups.
It was also observed that adolescents with central obesity presented significantly higher levels of TG at 4 hours, insulin and HOMA-IR, than adolescents without this comorbidity. Moreno et al.
] found that adolescents with central obesity had higher TG levels post-prandially compared with those with a peripheral pattern of fat distribution. Another interesting finding in the present study was the correlation between waist circumference and TG at 4 hours (rather than fasting TG), which corroborates the study by Rie Oka et
] that evaluated 1.505 men and 798 women aged 38-65 years and concluded that postprandial TG has a better relationship with waist circumference than fasting TG.
In the present study, it was also shown that only the adolescents with excess weight and fasting hypertriglyceridemia presented significant differences between the baseline and post-prandial TG values. In the postprandial state the persistent elevation of lipoproteins, rich in TG, can cause endothelial dysfunction, less availability of nitric oxide and increase of oxidative stress [18
]. Couch et al.
] studied the postprandial TG response to a fat load in children and their mothers from families with or without a family history of premature CHD (Columbia University Biomarkers Study) and found that a significantly greater postprandial TG response occurs in children with elevated fasting TG levels.
Nakajima et al. [20
] evaluated 23 overweight to obese adult volunteers and demonstrated a stronger correlation between plasma TG and remnant lipoprotein triglyceride (RLP-TG) in the postprandial state than in the fasting state. This study suggests that non fasting TG measurements could replace direct measurement of remnant lipoproteins for the assessment of cardiovascular disease risk.
In this group of adolescents with excess weight and fasting hypertriglyceridemia, the post prandial levels increased significantly up to the fourth hour. This fact did not occur in the eutrophic adolescents with fasting hypertriglyceridemia. Humans rarely consume a single meal during the day [21
]. Consumption of a subsequent meal causes a higher TG concentration than that which occurs after the first meal, even if the two meals are identical. As a result of this “second meal effect” the TG released can contain a significant amount of lipid from the previous one [21
]. Subjects with obesity, diabetes mellitus and metabolic syndrome present postprandial hyperlipidemia [22
]. One of the proposed mechanisms involves the competition between endogenous and exogenous TG-rich lipoproteins (TRLs) at different TG catabolic sites by overproduction of very low-density lipoproteins (VLDL) in the liver, in part due to hepatic insulin resistance [23
]. Umpaichitra et al.
] studied adolescents aged 10-19 years old with or without type 2 diabetes mellitus (obese and non-obese). They found that postprandial hyperlipidemia in response to a fat loading test is present in adolescents with type 2 diabetes mellitus who already have fasting hypertriglyceridemia.
In this study, no alteration was observed in the post-prandial levels of TC and LDL in the adolescents with excess weight and eutrophic adolescents. It has been well established that the ingestion of a meal rich in fats causes and increase in plasma triglycerides, whereas the concentrations of cholesterol are not significantly changed [25
One of the difficulties in establishing and using the measurements of post-prandial lipemia in daily clinical practice is the lack of an easy to use methodological protocol for general use. In the pediatric population, there is no consensus as regards the type of food, quantity of fat ingested, time of collection after overload and normal values after lipid overload. The protocol used in the present study has the advantage of being sufficiently simple, both from the point of view of preparation and duration, using products to which there is easy access in any country. The “shake” offered contained 25 grams of fat, considering that a typical daily pattern includes about 3-4 meals and each meal can contain 20-40 g of fat [26
]. In addition, the 4-hour duration protocol has been justified by previous studies [27
] that have investigated postprandial lipemia and shown that the fourth hour after fat load test is the most representative time to measure the TG response. The Expert Panel Statement [26
] suggests that a single TG measurement at 4 h after a fat loading test may represent a good estimation of the postprandial TG response.
The alterations resulting from the increase in lipoproteins do not depend only on their elevation (quantitative), but also on the qualitative characteristics of the diet (saturated, polyunsaturated and monounsaturated fats). Saturated fatty acids, with the exception of Stearic acid, increased the serum levels of all lipoproteins, particularly LDLc, since they reduce the synthesis and activity of the LDLc receptors by diminishing the expression of RNAm and membrane fluidity [29
]. It has been suggested that the ingestion of saturated fat is the main dietary cause of elevation of plasma cholesterol [30
]. A possible explanation for the absence of post-prandial elevation of LDLc and TC in the studied adolescents was the small quantity of saturated fatty acid used in the experiment (10.7% - 2.7 g/100 ml). In addition, the quantity of polyunsaturated fatty acid used (28.6% - 7.2 g/100 ml), may have influenced the LDLc and HDLc levels, because not only do polyunsaturated fats reduce LDLc, but they also reduce HDLc, thus inducing greater lipid oxidation [30
]. Monounsaturated fats are as effect in the reduction of TC as are polyunsaturated fats, however, without causing lipid oxidation and reduction in HDL concentrations. In the shake offered to the studied adolescents, the largest proportion of fat (60.7% - 15.2 g/100 ml) was monounsaturated fatty acid.
A meal that contained up to 15 g of fat was associated with minimal (20%) increases in post prandial TG peak levels, whereas high-fat meals (e.g., 50 g), including those served in popular fast-food restaurants, increased triglyceride levels by at least 50% beyond fasting levels [31
]. Approximately one out of five children with a BMI above the 95th percentile is hypertriglyceridemic, a rate that is 7-fold higher than for nonobese children of 6 to 10 years of age [31
]. The genetic abnormalities of triglyceride metabolism that may be identified in childhood are rare and generally diagnosed soon after birth. More commonly identified are milder triglyceride level elevations (ie, 100 to 500 mg/dL) due to obesity, the major cause of pediatric hypertriglyceridemia [31
]. Therefore, the prime target in counseling young children and their parents should focus on fat quality and quantity and then, in the early detection of underlying dyslipidemia [26
The strengths of this study include its large sample size, measurements of fasting, 2 and 4 hours postprandial TG levels on the same day in each individual. The test drink studied here has been shown to be palatable and acceptable to adolescents, and it provides reproducible evaluation of post-challenge triglyceride profiles. In this study the nutrient intake (in terms of calories) was comparable to meals commonly consumed in typical fast-foods all over the world.
In conclusion, the behavior of lipoproteins in the post-prandial state in eutrophic adolescents and those with excess weight is similar. Thus, apparently the weight excess does not induce post prandial lipemic alterations.