Many of the signals that result in a decrease in food intake in the short-term are activated by gastrointestinal (GI) responses to food ingestion and are transmitted to feeding centers in the brain, primarily via the vagus nerve. The interactions between the gut and the food ingested depend on the mac-ronutrient composition of the food. In addition to being populated by receptors that respond to the physiochemical properties of food, the gut has evolved to recognize the composition of the food ingested and to send signals in anticipation of their metabolic effects by release of peptide hormones to different organs involved in the processing of the nutrients derived from digestion and absorption . Whereas long-term food intake is controlled by adiposity signals, the regulation of short-term food intake is dictated mainly by food signals arising from both their preabsorptive action in the gut and their postabsorptive metabolism.
The ingestion of food and the passage of its subsequent digestion products through the GI tract prior to absorption gives rise to a myriad of signals that are transmitted to the brain, primarily by the vagus nerve, and are integrated with long-term energy signals to ensure an appropriate food intake response . Mechanoreceptors, osmoreceptors and chemoreceptors in the stomach and the small intestine provide direct signals to the brain. In addition, nutrients stimulate the release of GI hormones that act directly on receptors in the vagus nerve and in the brain.
Slower gastric emptying is associated with increased satiety . Many factors contribute to the rate of emptying, including the physical state and temperature of the meal, volume ingested, osmolality, caloric content, released digestive products and hormonal interactions. Solid foods are emptied more slowly from the stomach than liquid, increased volume accelerates the rate of gastric emptying, and solutions of high osmolality slow gastric emptying. However, while gastric distension contributes to food intake regulation, it alone cannot explain the state of satiety that typically lasts for several hours after a meal .
The secretion of hormones controlling food intake is regulated by the presence of food in the GI tract. The gut is a source of numerous peptides that contribute to the regulation of intake and metabolism. These include, from the small intestine, cholecystokinin (CCK), glucagon-like peptides (GLPs) 1 and 2, bombesin, gastrin-releasing peptide, neuromedin B, glucagon, apolipoprotein A-IV, amylin, somatostatin, enterostatin and peptide YY (3-36) and from the stomach, ghrelin and leptin [7, 11]. Many of the GI hormones and/or their receptors are also expressed in the central nervous system, underlining their important role in appetite control . Some enter the central circulation via leaky areas (brainstem and hindbrain) in the blood-brain barrier, or send signals through vagal afferents that are relayed to the hypothalamus. The macronutri-ent-dependent release of gut hormones might explain, at least in part, differences in the satiating and satiety effect of macronutrients. For example, fat and protein are the main CCK secretagogues in humans and rats, respectively , whereas carbohydrate and fat are stronger stimulants of GLP-1 release .
While the emergence of knowledge of the multiple satiety signals arising from the GI tract adds to the understanding of intake control, it has not yet led to an integrative picture of the action of these peptide hormones or to an understanding of their relative importance in response to food ingestion. Similarly, the role of postabsorptive signals remains unclear.
Postabsorptive signals are generated after nutrients have been digested and have entered the circulation where they stimulate satiety centers in the brain by endocrine and metabolic actions. The glucostatic, aminostatic and lipostatic hypotheses of intake regulation have been the main theories describing how absorbed nutrients generate and influence satiety signals .
The glucostatic theory postulates that fluctuations in blood glucose levels trigger an appropriate change in food intake. In support of the hypothesis, transient declines in blood glucose of the correct magnitude and time course have been associated with meal initiation as they are detected by peripheral and central glucoreceptive elements.
Similar to the glucostatic theory, the aminostatic hypothesis is based upon the brain monitoring of nutrients, in this case amino acids derived from protein ingestion, and consequently shaping consumption patterns. An inverse relationship between serum amino acid concentration and appetite in humans has been observed. It has been further postulated that amino acids act on food intake regulation through their ability to act as precursors to certain neurotransmitters known to influence food consumption. But as reviewed elsewhere, this may be a mechanism determining later food selection and the inter-meal interval rather than within meal satiation .
The lipostatic theory, advanced over 50 years ago, was based on signals arising from the metabolism of fats. In recent years, new evidence has emerged to support the hypothesis. Transport mechanisms and enzymes for both fat oxidation and synthesis are present in the brain and inhibitors of fatty acid oxidation increase food intake. Although this could be a peripheral effect, it is clear that the hypothalamus senses a nutrient surfeit in fatty acid metabolism arising from circulating lipids from either dietary sources or adipose tissue .
In addition to glucose, fatty acids and amino acids, a number of intermediate products of metabolism associate with satiety. Ketones, lactate, and pyru-vate suppress food intake in animals .
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