Metabolic and Lifestyle Determinants of Postprandial Lipemia Differ From Those of Fasting Triglycerides

Sharrett, A. Richey; Heiss, Gerardo; Chambless, Lloyd E.; Boerwinkle, Eric; Coady, Sean; Folsom, Aaron R.; Patsch, Wolfgang

doi:10.1161/01.atv.21.2.275

Cited by 78 publications

(63 citation statements)

References 43 publications

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“…Furthermore, the APOE3/2 genotype was associated with a greater variability in the postprandial responses. Fasting triacylglycerol concentration was associated with postprandial triacylglycerol response consistent with earlier reports in a population-based sample (Sharrett et al, 2001) and in subjects with type II diabetes (Reznik et al, 2002). It is suggested that dietary sucrose could increase synthesis and secretion of APOB (Abraham et al, 1994;Hellerstein, 2002).…”

Section: Discussionsupporting

confidence: 85%

Moderate increase in dietary sucrose does not influence fasting or postprandial serum lipids regardless of the presence of apolipoprotein E2 allele in healthy subjects

et al. 2007

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Objective: To investigate whether a moderate increase in dietary sucrose intake induces different serum lipid responses in normolipidemic subjects with the e2 allele compared with subjects without the e2 allele. Design: Controlled, parallel study. Subjects: There were 15 subjects with the apolipoprotein E (APOE)3/2 genotype and 19 subjects with the APOE3/3 or 3/4 genotype, whose mean7s.d. age was 48714 and 35710 years, respectively. All subjects had normal glucose metabolism. Interventions: The subjects were instructed to increase their sucrose intake by 40 g/day for 8 weeks and to decrease the intake of saturated and unsaturated fat to maintain energy balance. Dietary adherence was monitored using food records and the actual increase in sucrose intake was 39.8718.4 g/day. Sixteen subjects (nine with APOE3/2 genotype, seven with APOE3/3 or 3/4 genotypes) participated also in an 8 h oral fat tolerance test at the beginning and at the end of the intervention. Results: Body weight remained stable during the intervention. Sucrose intake did not have a significant effect on fasting concentrations of serum total and lipoprotein lipids, plasma glucose, serum insulin, squalene and non-cholesterol sterols in either genotype group. Neither were there any changes in postprandial lipid or insulin responses. Conclusions: Moderate increase in sucrose intake does not affect fasting or postprandial serum lipid responses in healthy subjects with or without the e2 allele.

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Section: Discussionsupporting

confidence: 85%

Moderate increase in dietary sucrose does not influence fasting or postprandial serum lipids regardless of the presence of apolipoprotein E2 allele in healthy subjects

et al. 2007

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“…In that case, a similar standardized test meal is to be used in every subject. (Weintraub et al, 1988(Weintraub et al, , 1989Lopez-Miranda et al, 1997Patsch et al, 1992;Mekki et al, 1999;Minihane et al, 2000;Tiret et al, 2000;Sharrett et al, 2001;Robertson et al, 2002;Jackson et al, 2003;Harbis et al, 2004).…”

Section: Aim Of Postprandial Lipaemia Testsmentioning

confidence: 99%

“…Fasting parameters (triglyceridaemia, cholesterolaemia, glycaemia) can be moderately elevated but with absence of any drug therapy. Compared with healthy subjects who demonstrate wellregulated lipid homeostasis, these subjects can be especially sensitive to meal challenges (Patsch et al, 1983;Mekki et al, 1999;Sharrett et al, 2001;Finnegan et al, 2003).…”

Section: Subjects At Disease Risk or Patientsmentioning

confidence: 99%

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Methodology for studying postprandial lipid metabolism

2007

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Background: Postprandial lipid metabolism in humans has deserved much attention during the last two decades. Although fasting lipid and lipoprotein parameters reflect body homeostasis to some extent, the transient lipid and lipoprotein accumulation that occurs in the circulation after a fat-containing meal highlights the individual capacity to handle an acute fat input. An exacerbated postprandial accumulation of triglyceride-rich lipoproteins in the circulation has been associated with an increased cardiovascular risk. Methods: The important number of studies published in this field raises the question of the methodology used for such postprandial studies, as reviewed. Results: Based on our experiences, the present review reports and discuss the numerous methodological issues involved to serve as a basis for further works. These aspects include aims of the postprandial tests, size and nutrient composition of the test meals and background diets, pre-test conditions, characteristics of subjects involved, timing of sampling, suitable markers of postprandial lipid metabolism and calculations. Conclusion: In conclusion, we stress the need for standardization of postprandial tests.

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“…Lifestyle and diet are, therefore, the major determinants of the phenotypic expression of major changeable risk factors (systemic arterial hypertension, dyslipidemia and diabetes). A recent study 22 has emphasized that smoking and diet were the major risk factors responsible for postprandial hyperlipemia, which is known to be a condition associated with the atherosclerotic process. An improvement in these determinants is associated with better control of these risk factors and a reduction in the incidence of the coronary artery disease 23 .…”

Section: Discussionmentioning

confidence: 99%

Distribution of risk factors in parents and siblings of patients with early coronary artery disease

Mansur¹,

Mattar

Rolim

et al. 2003

Arq. Bras. Cardiol.

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Original ArticleCoronary artery disease is the major cause of death in the Brazilian population 1 and is directly related to the number and intensity of risk factors 2 , which may be generically divided into unchangeable (age and sex) and changeable. The major changeable risk factors are obesity, sedentary lifestyle, systemic arterial hypertension, smoking, dyslipidemia, and diabetes. Smoking and sedentary lifestyle are basically behavioral, and the remaining risk factors are associated with genetic and environmental components. Studies in different populations have shown the greater importance of environmental and behavioral components in the genesis of the atherosclerotic process 3 . A classical example is the greater prevalence of the disease in individuals migrating from a more favorable environment to one with a more atherogenic profile 4 . Likewise, some studies 5,6 have shown the importance of the microenvironment, in particular the family, where genetic influences and lifestyle are equally important. Offspring of parents with systemic arterial hypertension or with dyslipidemia have a greater incidence of diseases whose phenotypes are influenced by the familiar lifestyle. The result of this interaction is responsible for atherosclerotic disease, which normally affects males after the 6th decade and females almost 1 decade later 7 . In younger patients with coronary artery disease, a greater participation of the genetic component has been discussed. Despite the existing controversies, a familiar analysis may directly or indirectly facilitate the detection and quantification of which component, genetic or environmental, has the greatest impact on early atherosclerotic disease, and, consequently, on its future control. Therefore, the major objective of this study was to analyze the prevalence of risk factors in families of patients with early systemic arterial disease, and to detect the importance of parents in the vertical transmission of these risk factors. MethodsThis study prospectively analyzed the distribution of the major risk factors of parents and siblings of 42 conse- 102 RF,4,3,2, and 1 were observed in, respectively,5,15,15,and 7 Objective -Early coronary artery disease (CAD) is associated with risk factors (RF). Offspring of parents with a RF have a greater prevalence of them. However, the distribution of RF in parents and siblings of patients with early CAD is unknown. Methods -The study comprised the parents and siblings of 42 patients with early CAD (≤ 45 years), 29 males. Their mean age was 39.5±3.7 years. The following major RF were analyzed: smoking (≥ 5 cigarretes/day), hypercholesterolemia (total cholesterol ≥ 200 mg/dL), hypertension (diastolic blood pressure ≥ 90 mmHg), and diabetes (glycemia ≥ 126 mg/dL). Results -Of a total of

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Metabolic and Lifestyle Determinants of Postprandial Lipemia Differ From Those of Fasting Triglycerides

Cited by 78 publications

References 43 publications

Moderate increase in dietary sucrose does not influence fasting or postprandial serum lipids regardless of the presence of apolipoprotein E2 allele in healthy subjects

Moderate increase in dietary sucrose does not influence fasting or postprandial serum lipids regardless of the presence of apolipoprotein E2 allele in healthy subjects

Methodology for studying postprandial lipid metabolism

Distribution of risk factors in parents and siblings of patients with early coronary artery disease

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