Wilson (1968) showed essentially all tissues in the body of the squirrel monkey have the capacity to synthesize cholesterol.
The typical diet of Western humans is rich in fat and cholesterol, and both constituents are believed to contribute to the coronary heart disease (CHD) epidemic in Western societies. Many studies have been conducted in nonhuman primates (reviewed in Strong, 1976) using diets imitating the Western diet to identify the nutritional factors important in development of atherosclerosis (hardening of the arteries), the disease process underlying CHD and the leading cause of death in Western societies (Marmot, 1992). When diets are fed containing 35-40% of ME as fat of different types, nonhuman primates do not develop significant atherosclerosis. However, when cholesterol is added to such diets, most species develop a degree of hypercholesterolemia that is species-specific (Rudel, 1997). Studies of the sensitivity of Macaca to dietary induction of atherosclerosis have included the rhesus monkey (Macaca mulatta), cynomolgus monkey (Macaca fascicularis), and pigtailed macaque (Macaca nemestrina) (Strong, 1976). Macaques, in general, are highly diet responsive, with cynomolgus monkeys and pigtailed macaques being particularly sensitive. Vervet monkeys (Cercopithecus aethiops) and patas monkey (Erythrocebus patas) are less so and require more dietary cholesterol to induce hypercholesterolemia and atherosclerosis (Rudel, 1997). The baboon (Papio spp.) has been extensively studied, is among the most diet-resistant primate species, and requires a dietary cholesterol concentration of 1.7 mg·MEkcal-1 for atherosclerosis to develop (McGill et al., 1981). If nonhuman primates are maintained on a hypercholesterolemic diet long enough, usually several years, coronary artery atherosclerosis will develop (Rudel et al., 1995a), and the coronary artery lesions will show essentially all of the characteristics seen in atherosclerosis in humans (Rudel et al., 1995b). Nonhuman-primate diets enriched in n-3 and n-6 polyunsaturated fatty acids appear to protect against coronary arterial atherosclerosis, whereas diets enriched in saturated and monounsaturated fatty acids appear to promote the disease, as demonstrated in several studies (Rudel et al., 1995a; Rudel et al., 1995b; Rudel et al., 1998; Wolfe et al., 1994). The phytoestrogen content of soy is protective, and the primate model has been useful in clarifying these effects (Anthony et al., 1997; Clarkson et al., 2001).
The lesson to be taken from those studies is that many species of nonhuman primates have a diet-related susceptibility to atherosclerosis similar to that of humans and so can constitute good models for studying the mechanisms of atherosclerosis. In general, these man-prepared diets are well tolerated; and in some studies in which offspring were born and raised, body weight and size were normal to large relative to those of comparable animals from the wild (Wolfe et al., 1993). However, the likelihood that such diets would be encountered in the wild by nonhuman primates is nil.
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