Postprandial Hyperlipidemia after a Fat Loading Test in Minority Adolescents with Type 2 Diabetes Mellitus and Obesity

Umpaichitra, Vatcharapan; Banerji, Mary Ann; Castells, Salvador

doi:10.1515/jpem.2004.17.6.853

Cited by 27 publications

(27 citation statements)

References 11 publications

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“…The increased triglyceride levels during the fat-loading tests observed in our study are consistent with findings reported by others (37)(38)(39) and have been discussed previously (40). The relationship between elevated PAI-1, insulin resistance, and hypertriglyceridemia is established (2,6,17,18,36,41) and is shown in our study.…”

Section: Discussionsupporting

confidence: 93%

Plasminogen Activator Inhibitor-1 and Tissue-Plasminogen Activator in Minority Adolescents with Type 2 Diabetes and Obesity

2005

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Increased plasminogen activator inhibitor-1 (PAI-1) and decreased tissue-plasminogen activator (t-PA) activities lead to impaired fibrinolysis, which is critical for cardiovascular disease. We studied these hemostatic factors at fasting state and after an oral fat load in 12 type 2 diabetic and 17 nondiabetic obese adolescents, matched for age, sex, body mass index, and sexual maturation. Plasma PAI-1, t-PA, and glucose as well as serum C-peptide, insulin, total cholesterol, triglyceride, and HDL and LDL cholesterol levels were measured at 0, 2, 4, and 6 h after the fat load. Metabolic responses were expressed as the area under the curve (AUC). PAI-1 activities were significantly greater in patients than in control subjects [fasting, 23.4 Ϯ 2.6 versus 12.9 Ϯ 2.0 U/mL (p Ͻ 0.004); AUC, 101.7 Ϯ 12.1 versus 57.6 Ϯ 6.5 U · h Ϫ1 · mL Ϫ1 (p Ͻ 0.003)]. Fasting t-PA activities were significantly lower in the patients than in the control subjects (0.8 Ϯ 0.3 versus 6.5 Ϯ 2.7 U/mL; p Ͻ 0.001). Triglyceride was the only lipid parameter that was significantly different in the patients than in the control subjects [fasting, 1.5 Ϯ 0.2 versus 0.9 Ϯ 0.1 mM (p Ͻ 0.05); AUC, 15.7 Ϯ 2.9 versus Insulin resistance followed by absolute or relative insulin deficiency is a known course of type 2 diabetes development (1,2). Type 2 diabetes, obesity, dyslipidemia, and abnormal factors related to blood clotting are risk factors of cardiovascular disease (CVD) and are often seen in patients with insulin resistance (2-7). Tissue-plasminogen activator (t-PA) initiates fibrinolysis. Plasminogen activator inhibitor-1 (PAI-1) binds rapidly to t-PA and has an inhibitory activity against t-PA (6). As a result, abnormal PAI-1 and/or t-PA activities contribute to a thrombotic tendency (6). Elevated plasma PAI-1 activities and antigens have been reported in adults with type 1 diabetes, type 2 diabetes, and obesity as well as in children with type 1 diabetes and obesity (8 -20). Elevated plasma t-PA antigens have been reported in adults with type 1 diabetes, type 2 diabetes, and obesity as well as in children with type 1 diabetes and obesity (8,13,19,21). Decreased plasma t-PA activities and a decreased capacity of endothelial cells to secret t-PA in response to a fibrinolytic stimulus were also reported in adults with diabetes (7,14,22). Normal PAI-1 and t-PA antigens, however, have been shown in children and adults with type 1 diabetes (17,19). Because there are few data about PAI-1 and t-PA in children and adolescents with type 2 diabetes, there is a continuing increase in type 2 diabetes and obesity in this population, which is thought to be due to high caloric intake and sedentary life style (especially in minority groups) (23)(24)(25), and CVD begins in childhood (26,27), we studied the PAI-1 and t-PA activities at fasting state as well as an impact of a fat load assigned to simulate the fat content of a high-fat, fast-food meal (28) to these critical factors in minority adolescents with type 2 diabetes and obesity.

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Section: Discussionsupporting

confidence: 93%

Plasminogen Activator Inhibitor-1 and Tissue-Plasminogen Activator in Minority Adolescents with Type 2 Diabetes and Obesity

2005

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“…These estimates are broadly consistent with previous cross-sectional studies that have found significant differences in PPL when assigning 8-15 subjects per group (Gill et al 2004;Umpaichitra et al 2004). Nevertheless, we acknowledge that it is possible that a larger absolute difference in body composition, i.e.…”

Section: Discussionsupporting

confidence: 90%

“…However, TG levels returned to baseline values at 6 h in the NW group but were still elevated at 6 h in the OW group, suggesting a delayed clearance. Coupled with the correlations of sum of skinfolds with TG AUC, and previous evidence showing greater postprandial TG responses to a high-fat meal in obese adolescents and adults (Gill et al 2004;Moreno et al 2001;Umpaichitra et al 2004), there remains the possibility that OW adolescents are at greater risk of postprandial exposure to atherogenic particles. The mechanisms responsible for the exercise-induced reduction in PPL in the present study have not been fully characterized.…”

Section: Discussionmentioning

confidence: 99%

“…It is not uncommon for adolescents in industrialized nations to spend considerable time in the postprandial state in a typical day and there is now compelling evidence that atherosclerotic processes begin early in childhood and are influenced over the life course by genetic and potentially modifiable risk factors, such as exercise (Glowinska et al 2003;Sorenson et al 1994). Investigations of the postprandial triglyceride response in adolescents have been primarily limited to observational examinations of the influence of fat distribution and growth hormone deficiency (Lanes et al 2004;Moreno et al 2001;Umpaichitra et al 2004). Barrett and colleagues have previously investigated the effect of physical activity on PPL in adolescents and reported a *20% reduction in postprandial TG after continuous and intermittent moderate activity (Barrett et al 2007;Tolfrey et al 2008).…”

Section: Discussionmentioning

confidence: 99%

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Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys

et al. 2009

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Postprandial lipemia (PPL) is associated with impaired endothelial function and inflammation. Acute exercise reduces PPL in adults. This investigation examined the effect of an acute bout of exercise on postprandial changes in triglycerides (TG), glucose, insulin, inflammation [white blood cell count (WBC), interleukin-6 (IL-6) tumor necrosis factor-alpha, C-reactive protein (CRP)] and endothelial activation [soluble intercellular adhesion molecule-1 (sICAM-1), vascular adhesion molecule-1 (sVCAM-1)] following a high-fat meal in adolescents. Ten normal weight (NW) (BMI, 20.9 +/- 1.7 kg m(-2); 15.6 +/- 0.7 years) and eight overweight (OW) (BMI, 28.3 +/- 3.6 kg m(-2); 15.9 +/- 0.4 years) adolescent boys underwent two 6-h oral fat tolerance tests (OFTT) separated by 7-10 days. On the evening prior to each OFTT, subjects either rested or completed a treadmill exercise bout (65% V(O)(2max); 600 kcal expended). Exercise reduced (P < 0.01) the postprandial TG area under the curve by approximately 20% in the NW and OW groups. The postprandial glucose and insulin response did not differ between the control and exercise trials or between the NW and OW groups. Circulating leukocytes and plasma IL-6 levels increased (P < 0.01) in the NW and OW groups 6 h following the OFTT in both experimental conditions. There were no changes in CRP, sVCAM-1 or sICAM-1 following the OFTT and there were no differences between experimental condition or NW and OW groups. In conclusion, a moderate exercise bout prior to a high-fat meal effectively reduces postprandial TG concentrations to a similar degree in both NW and OW adolescents, but does not reduce the concomitant postprandial increase in WBC or IL-6.

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“…The several OTTT protocols that have been investigated include those that vary fat intake according to body weight (1 g dairy cream/kg body weight) as well as those that use a fixed combined challenge (50 g fat plus 50 g carbohydrate) (14 ). In controlled studies of healthy individuals, as well as those with metabolic syndrome or diabetes, methods that measure blood concentrations 2-4 h after the administration of calibrated fat loads have proved to be reproducible and palatable approaches for assessing postchallenge triglyceride concentrations (14,15 ).…”

mentioning

confidence: 99%

Fasting versus Nonfasting Triglycerides and the Prediction of Cardiovascular Risk: Do We Need to Revisit the Oral Triglyceride Tolerance Test?

Ridker

2008

Clinical Chemistry

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Historically, triglycerides have been measured in the fasting state for 2 reasons. First, because of the marked increase in triglycerides after fat ingestion, the variability in triglyceride measurements is much smaller in the fasting state. Second, before the availability of direct assays for LDL cholesterol (LDL-C), 1 estimation of LDL-C was performed in clinical practice almost exclusively by use of the Friedewald equation, which requires that both the HDL-C concentration and the fasting triglyceride concentration divided by 5 be subtracted from the total cholesterol concentration.The recommendations to measure triglycerides in the fasting state did not, however, derive from a consistent set of prospective cohort studies showing that fasting concentrations were superior to nonfasting concentrations for the detection of cardiovascular risk. Instead, following screening guidelines, most epidemiologic investigations simply relied on fasting triglycerides. Taken as a whole, such studies indicate that fasting triglycerides are a univariate predictor of vascular disease. Controversy exists, however, regarding the clinical usefulness of fasting triglycerides as an independent predictor of risk, because adjustment for other covariates-in particular HDL-C-markedly decreases both the magnitude and significance of observed epidemiologic effects (1 ). The extent to which investigators have sought to avoid nonfasting triglycerides as a method for risk detection is evident in a recent metaanalysis that limited evaluation only to those epidemiologic studies that measured fasting triglycerides, specifically "to exclude the possibility of postprandial effects" (2 ).Is it possible, then, that recommendations to measure triglycerides in the fasting state have systematically underestimated the impact of hypertriglyceridemia in clinical practice? Atherosclerosis has long been hypothesized to be a disorder influenced by postprandial effects. As early as 1950, J. R. Moreton, writing in the Journal of Laboratory and Clinical Medicine, suggested a linkage between chylomicronemia, fat tolerance, and atherosclerosis (3 ). A major source of circulating triglycerides is dietary fat, which, after hydrolysis into free fatty acids and glycerides, is transported through the intestinal villi and absorbed by enterocytes, where these particles are synthesized into chylomicron-associated triglycerides for entry into the blood compartment and ultimately storage in adipose tissue. Postprandial lipids and their associated partially hydrolyzed chylomicron remnants appear to promote early atherogenesis, adversely affect endothelial function, associate with atherogenic small LDL particles, and correlate with both prothrombotic and proinflammatory biomarkers, including factor VII, plasminogen activator inhibitor-1, and C-reactive protein (4 ). Thus, measurement of postprandial triglycerides-particularly because they peak 3-4 h after ingestion of a fat-rich mealmight well provide more relevant information on vascular risk than measurements based on fast...

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Postprandial Hyperlipidemia after a Fat Loading Test in Minority Adolescents with Type 2 Diabetes Mellitus and Obesity

Cited by 27 publications

References 11 publications

Plasminogen Activator Inhibitor-1 and Tissue-Plasminogen Activator in Minority Adolescents with Type 2 Diabetes and Obesity

Plasminogen Activator Inhibitor-1 and Tissue-Plasminogen Activator in Minority Adolescents with Type 2 Diabetes and Obesity

Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys

Fasting versus Nonfasting Triglycerides and the Prediction of Cardiovascular Risk: Do We Need to Revisit the Oral Triglyceride Tolerance Test?

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