The regulation of food intake is a complex interaction between numerous signals acting both peripherally and centrally, each varying over time.
Consuming a meal may be divided into three phases: a pre-prandial, a prandial and a postprandial (pre-absorptive and post-absorptive) phase. In addition, food intake is usually divided into two phases: satiation (meal termination) and satiety (absence of satiety leads to meal initiation). Roughly speaking, factors important during the prandial phase are involved in satiation, and factors important during the postprandial phase are involved in satiety. However, in practice this distinction is less clear.
Satiation (meal termination)
During the pre-prandial phase, visual, olfactory, gustatory and tactile inputs stimulate processes at multiple sites (i.e. salivary glands, gastrointestinal tract, pancreas, and cardiovascular and renal systems). These processes result in a cascade of physiological processes, termed the 'cephalic phase response', which occurs within seconds to minutes after exposure to foods. The taste and smell of foods stimulate, for example, gastrin and gastric acid release (Mattes, 1997). The cephalic phase responses improve or optimize the efficiency of the digestion, absorption and utilization of nutrients (Halford and Blundell, 2000).
During the prandial phase the central nervous system receives sensory afferent inputs reflecting the amount of food eaten and initial estimations of its nutrient content. Mechanoreceptors in the gut detect the distension of the gut caused by the presence of food. This helps to estimate the volume of food consumed. Fullness is directly correlated to gastric content, and hunger and desire to eat are inversely correlated. Oral ingestion of a physiological amount of nutrients leads to the greatest suppression of appetite. Orosensory stimulation (taste and smell perception) enhances the appetite-suppressing effects produced by gastric distension, probably partly caused by slower gastric emptying (Cecil et al., 1998).
Chemoreceptors in the gastrointestinal tract detect the chemical presence of nutrients, and provide information on the composition of the foods consumed. Factors such as cholecystokinine (CCK) and glucagon-like peptide 1 (GLP-1) are released in response to the chemical presence of food in the gastrointestinal tract. CCK is a hormone released in the duodenum in response to consumption of fat (i.e. long-chain fatty acids) or protein (i.e. amino acids). GLP-1 is a hormone released in the blood by mucosal cells of the gut in response to the presence of carbohydrates and fat (Macintosh et al., 2001). CCK and GLP-1 suppress appetite by decreasing gastric emptying - by affecting the pyloric pressure, stomach motility and stomach muscle relaxation. By decreasing stomach emptying, the stomach distension increases, leading to sensations of fullness (Geliebter et al., 1988; Rolls et al., 1998). GLP-1 stimulates the islet B-cells in the pancreas to secrete insulin, thereby lowering blood glucose levels in response to carbohydrate consumption.
The effect of nutrients on satiety and satiation depends on the position of the nutrients in the digestive tract. The presence of physiological amounts of nutrients in the intestine provides a weak stimulus for the regulation of appetite. The same physiological amount of nutrients in the stomach leads to an increased suppression of appetite.
Satiety (meal initiation)
Owing to its central role in the regulation of energy metabolism, the role of glucose in meal initiation has been extensively investigated. Although absolute concentrations of glucose do not seem to be very important in the regulation of food intake (Chapman, 1998; Gielkens et al., 1998), transient and dynamic declines in blood glucose concentration seem to be strongly related to meal initiation (Campfield and Smith, 1990; Kovacs et al., 2002). In addition, intraduodenal glucose influences appetite, possibly through glucoreceptors or osmoreceptors in the intestine, which may induce satiety through direct vagal stimulation or via the release of insulin and/or incretin hormones such as GLP-1 (Lavin et al., 1996). Unlike glucose, the role of insulin in the regulation of food intake is not clear, since studies examining exogenous insulin as well as studies investigating endogenous insulin give mixed results (Campfield et al., 1996; Chapman, 1998).
Ghrelin is abundantly synthesized in the fundus of the human stomach (Ariyasu et al., 2001), and is suggested to be involved in meal initiation. Plasma ghrelin concentrations rise before each meal and they decrease between meals (Cummings et al., 2002). Moreover, an intravenous infusion of ghrelin in humans has been shown to increase food intake potently and enhance appetite by approximately 28% (Wren et al., 2001). In response to oral and intravenous administration of glucose, plasma ghrelin concentrations decrease. Intake of an equivalent volume of water, however, does not influence ghrelin concentrations (Shiiya et al., 2002), suggesting that secretion of ghrelin is not affected by stomach expansion. Moreover, ghrelin responses are dependent on energy dose and on type and composition of the macronutrients (Blom et al., 2005, 2006). Ghrelin concentrations appear to be positively associated with appetite scores and inversely associated with intermeal interval. Such associations suggest that suppression of ghrelin concentrations may postpone initiation of the next meal. These are interesting results that need to be investigated further.
Peptide YY (PYY), which is also a gut hormone, is postprandially released in response to medium- and long-chain fatty acids but not after sucrose polyester ingestion (Maas et al., 1998). PYY suppresses 24-h food intake in humans (Batterham et al., 2002) and is correlated with measures of appetite (MacIntosh et al., 1999).
Long-term food intake regulation is essential in food-weight management. The hormone leptin appears to be involved in long-term food intake regulation. Leptin is synthesized mainly by adipose tissue; it acts through receptors present in afferent visceral nerves and the hypothalamic arcuate nucleus, whose neurons are capable of expressing and releasing neuropep-tide Y and agouti-related protein which activate ingestive behavior through the paraventricular nucleus.
Plasma leptin concentrations correlate positively with total body fat stores (Sinha et al., 1996). An energy deficit of more than 24 h leads to decreases of plasma leptin concentration (Boden et al., 1996), whereas an energy surplus of more than 24 h results in increased leptin concentrations (Kolaczynski et al., 1996). Plasma leptin is negatively correlated with appetite and food intake when the energy balance is severely disturbed (Keim et al., 1998; Chin-Chance et al., 2000).
When subjects are in energy balance, the relation between leptin concentrations and food intake and appetite is less clear (Karhunen et al., 1997; Joannic et al., 1998; Romon et al., 1999). Therefore, leptin seems to have a role in the regulation of food intake when energy stores are depleted or increased, rather than during energy balance.
The balance and interaction between anorexigenic (e.g. CCK, PYY) and orexigenic (ghrelin) factors originating from the gastrointestinal tract appear to play an important role in short-term regulation of food intake. An impairment of this balance may result in disorders of feeding behavior and weight gain (obesity) or weight loss (cachexia). Understanding this balance is essential in developing foods that help people maintain a healthy body weight.
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