Food and its components contribute to both short- and long-term regulation of food intake. The challenge is to understand the relative importance of food components and how to optimize their interaction with intake regulatory systems.
At the physiological level, energy requirement is a powerful determinant of food intake . Thus growth, increased activity, and exposure to cold increase intake. Physiological systems in both experimental animals and humans are remarkably precise in regulating energy intake in relation to requirements. For example, exposure to cold or to exercise, or alterations in the energy density of the diet or to food availability and choice result in rats quantitatively adjusting their food intake, thus maintaining energy balance when provided with their usual diets [14, 17]. However, it is also clear that experimental animals will become obese when provided a variety of palatable foods, or high fat diets, showing that factors other than the physiological drive toward energy balance determine food intake .
Similarly, humans adjust their energy intake to meet their energy expenditure in response to changes in activity, or ambient temperatures. As with experimental animals, humans consume excess energy when they are exposed to an environment of low activity  and highly palatable energy dense foods .
Although all macronutrients provide energy, their effect on food intake cannot be predicted simply from their energy content. Each macronutrient possesses unique properties that provide signals to the central nervous system independent of their energy content .
Protein suppresses food intake more than carbohydrate, which in turn suppresses food intake more than fat. This hierarchy has been shown in both humans and rats . Less appreciated is that even within a macronutrient class, the source is a factor influencing short-term food intake and appetite. However, it is not possible at present to identify the primary biomarkers of satiety that arise from proteins, carbohydrates and fats.
The mechanisms by which proteins stimulate intake regulatory systems are many, making them unique compared with carbohydrates and fats. Furthermore, the systems stimulated are dependent on the source. The satiety cascade arising from protein is as follows. First, protein initiates satiety through its digestion and the subsequent release of biologically active peptides (BAP) encrypted within the protein. These BAP affect feeding through their actions in the GI tract. They activate receptors, thus providing signals via the vagus nerve either directly, or by interacting with gut hormones that are involved in intake regulation. Second, free amino acids arising from digestion activate neurochemical systems, thereby contributing not only to satiety, but also to macronutrient choice. Finally, the end products of amino acid metabolism, ammonia and urea, probably play a part in determining intervals between meals, but act primarily to signal excess intake or errors in metabolism .
Protein source, in addition to protein quantity, is a determinant of satiety . Greater subjective satiety was reported by young men fed a 50-gram meal of lean fish compared with an equivalent amount of either beef or chicken . Whey and soy protein drinks (45-50 g protein) suppressed food intake 1 h later compared with the energy-free control and with sucrose, whereas egg albumen did not .
The differential effect of protein source on food intake and subjective appetite might be explained by the action of BAP released during protein digestion. These peptides are unique to the protein source and dependent on its tertiary structure and amino acid composition. Among the most extensively studied BAP are those derived from milk digestion. A glycosylated form of caseinomacropeptide (GMP), a peptide derived from the in vivo and in vitro digestion of casein, is a potent CCK secretagogue , and preliminary studies from our laboratory show that GMP is a potent inhibitor of food intake in rats . In addition to GMP, opioid peptides derived from the digestion of casein (casomorphins) suppress food intake through opioid receptors located in the GI tract .
Consistent with the glucostatic hypothesis are the observations that carbohydrate consumption and the resulting increase in blood glucose are associated with satiety. In the short-term, high glycemic carbohydrates suppress food intake (up to 2 h) more than low-glycemic carbohydrates . Although there is much indirect support for the hypothesis that satiety is associated with the glycemic effects of carbohydrates, a primary role for blood glucose in determining satiety remains uncertain , perhaps because the glycemic response to carbohydrates primarily depicts their absorption characteristics. Many other mechanisms, including those based on the rate of gastric emptying and gut hormones, may explain the different effects on satiety of slow compared to rapidly digested carbohydrates. For example, a rapid increase in the stimulation of glucoreceptors would be expected following ingestion and digestion of carbohydrates, but this stimulation does not last long enough to account for the prolonged satiety effect. A more extended effect of carbohydrates on satiety could arise from the stimulation of a multitude of gut peptides, such as GLP-1 and CCK [28, 29]. Gastric emptying is slowed by GLP-1, a putative satiety peptide whose release is stimulated by carbohydrates in the small intestine and that regulates carbohydrate metabolism . A rise in blood glucose concentrations is also a factor that slows gastric emptying .
In general, fat suppresses food intake less than carbohydrate or protein on a calorie for calorie basis. However, this ranking may also depend on the source. Among fats, both the chain length and the degree of saturation have been shown to impact short-term food intake and subjective appetite. Medium-chain triglycerides and polyunsaturated fatty acids suppressed food intake more than long-chain triglycerides and monounsaturated or saturated fatty acids, respectively. These effects have been attributed to the CCK and apolipoprotein A-IV releasing properties of these types of fats .
It is clear that an understanding of the interaction between food components and the intake regulatory mechanisms continues to develop. However, as noted earlier, there is little information on the stability of the system once the development of the circuitry has been completed. Similarly lacking is information on the role of environmental or nutritional factors in the development of the intake regulatory system in utero and in early life.
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