Obesity is one of the major health risks for a number of diseases, particularly heart disease and diabetes. It is well known that ingestion of a diet high in saturated fats is one of the major causes of obesity. There are two explanations for this observation. First, diets high in saturated fats do not seem to be as satiating as either high-carbohydrate or highprotein diets (Doucet et al., 1998), even when the high-fat diet is less palatable (Warwick, 1996). Second, whereas increased intake of either carbohydrate or protein causes a concomitant increase in energy expenditure (e.g., nonshivering thermogenesis), increased intake of saturated fat does not cause a similar increase in energy expenditure. Individuals maintained for 1 wk on a high-carbohydrate or high-protein diet have, whereas individuals maintained on a diet high in saturated fat did not have, increased body temperature and ingested fat was mostly sequestered to adipose tissue; that is, increased intake of saturated fat does not promote the use of fat as a metabolic fuel (Schutz, Flatt, & Jequier, 1989; Thomas et al., 1992). Thus, diets high in saturated fats are more obesity producing than diets high in carbohydrate or protein because of their lesser ability to satiate appetite and to increase fat oxidation. With the ingestion of more energy than expended, storage of fat is increased and obesity results (Tremblay, Plourde, Despres, & Bouchard, 1989).
The peptide hormone insulin is produced in the pancreas and secreted in proportion to the degree of adiposity. Similar to leptin, insulin levels are correlated with amount of abdominal fat (Porte et al., 1998; Woods et al., 1996; Woods, Figlewicz Lattemann, Schwartz, & Porte, 1990; Woods et al., 1998). It is transported into the brain where it acts to decrease food intake and body weight (Schwartz, Figlewicz, Baskin, Woods, & Porte, 1992; Woods et al., 1996). High insulin resistance is a characteristic of obesity, hypertension, and non-insulin-dependent diabetes mellitus. There is an inverse relationship between insulin action and triglyceride content. With the ingestion of fat, insulin secretion is increased. Insulin stimulates fatty acid synthase, an enzyme that catalyzes all reactions involved in lipogenesis, and thereby results in the accumulation of triglycerides (Sul, Latasa, Moon, & Kim, 2000). Monounsaturated fatty acids (such as oleate) and saturated fatty acids (such as palmitate), fatty acids with little or no influence on fatty acid synthase, are incorporated into triglycerides in adipose tissue (Parrish, Pathy, & Angel, 1990; Parrish et al., 1991; Su & Jones, 1993) and thereby increase insulin resistance. In contrast, n-3 PUFAs markedly inhibit fatty acid synthase and are, therefore, preferentially incorporated into phospholipids for cell membrane remodeling; that is, n-3 PUFAs decrease triglyceride production, resulting in low levels of tissue and plasma triglycerides (see Fig. 5), and thereby decrease insulin resistance (Awad et al., 1990; Chicco et al., 1996; Hill et al., 1993; Parrish et al., 1991; Russell et al., 1991; Rustan et al., 1993; Sohal et al., 1992). Clearly, ingestion of diets high in n-3 PUFAs should be beneficial for treatment of obesity and diabetes. For maximal benefit, ingestion of diets with appropriate amounts of n-3 PUFAs should begin at an early age or possibly prolonged ingestion may be required.
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