Dietary fat has frequently been blamed for the increase in prevalence of obesity (Bray et al., 2004). Epidemiological studies have demonstrated a positive relationship between high-fat diets and excess energy intake due to their high energy density and palatability (Prentice and Poppitt, 1996). However, this association is confounded by differences in physical activity, smoking, and food availability and variety (Willett, 1998; Bray et al., 2004). Furthermore, epidemiological studies investigating the association between high fat intake and obesity have been inconsistent (Seidell, 1998; Willett, 1998). Preload studies have shown that fat exerts the weakest effect on satiety compared to carbohydrate and protein, suggesting that fat may lead to “passive overconsumption” (Blundell et al., 1993). But when preloads were matched for energy density and palatability, differences in satiety were not obvious (Geliebter, 1979; Stubbs and Harbron, 1996; McCrory et al., 2000), pointing to energy density as the key driver of satiety under experimental conditions. Furthermore, lipids suppress later food intake when present in the small intestine of both humans and animals (Welch et al., 1988; Greenberg et al., 1990; Drewe et al., 1992; Woltman and Reidelberger, 1995; Castiglione et al., 1998; Van Wymwlbeke et al., 1998). Relatively few studies have investigated the responses of specific fats and fatty acids on food intake. Furthermore, studies have used different fats and fatty acids making it almost impossible to draw conclusions. However, it is clear that not all fats are equal in their effect on appetite and associated biological processes.
