ABSTRACT
Metabolism ...................................................................572 22.2.7.2 Intraindividual Variation in Postprandial
Lipid Metabolism .......................................................... 574 22.2.8 Lipid Biochemical Pathways ......................................................... 574 22.2.8.1 MUFA ..........................................................................575 22.2.8.2 PUFA ............................................................................576 22.2.8.3 Omega-3 .......................................................................577 22.2.8.4 Omega-6 .......................................................................578 22.3 Fat and Diet ................................................................................................. 579 22.3.1 Lipids in Control of Food Intake ................................................... 579 22.3.2 Impact of a High-Fat Meal on Endothelial Function .................... 580 22.3.3 Effect of Varying Dietary Fatty Acid Composition
on Endothelial Function ................................................................ 581
22.3.3.1 MUFA ...........................................................................581 22.3.3.2 PUFA ............................................................................581 22.3.4 Long-Term and Acute Effects of Dietary Fat Content
and Composition on Postprandial Lipemia ................................... 582 22.4 Conclusions ................................................................................................. 582 Abbreviations ......................................................................................................... 585 References .............................................................................................................. 585
The prevalence of overweight and obesity today is unprecedented and is steadily and globally rising (Balkau et al., 2007). Why are so many apparently healthy individuals consuming more calories than they need? Variations in the development and consequences of obesity have been proposed to depend on genetic predisposition combined with various environmental factors that lead to a chronically unbalanced energy intake relative to its expenditure. The variables that could contribute to uctuations in body weight and composition have been proposed to include genetics (Corella and Ordovas, 2005; Warensjo et al., 2007; Benzinou et al., 2008; Masuo et al., 2008; Pichler et al., 2008); activity (Hill and Melanson, 1999), including nonexercise activity thermogenesis (Levine et al., 1999); diet composition (Labayen et al., 2003; Layman et al., 2003; Meckling et al., 2004; Cornier et al., 2005; Capel et al., 2008) and structure (BrandMiller et al., 2002; McMillan-Price et al., 2006); and metabolic phenotype (Cornier et al., 2005). There is also evidence that today’s “obesogenic environment,” which includes easy, 24 h access to high-energy foods, large portion sizes, and a social environment that promotes a sedentary lifestyle, is contributing to obesity (Poston and Foreyt, 1999). Yet, not all individuals become obese in response to this obesogenic environment, indicating that there is a strong genetic component involved in the development of obesity (Wardle et al., 2008). Individuals are different, and the causes and solutions for their overweight condition are therefore necessarily also different.
