Satiety Peripheral Physiological Influences

Intake of energy can only be achieved (in mammals) through the gastrointestinal tract, and energy intake is limited by the capacity of the tract. Humans are periodic feeders and usually meals are separated by periods (intermeal intervals) of 3-5 h during which little food is eaten. It can be noted that the periodicity of meal eating is compatible with the time taken by the gastrointestinal tract to process a meal. After the ingestion of a meal the stomach mixes the meal with gastric secretions that aid its liquefaction and delivers the mixture at a steady rate into the small intestine for further chemical digestion and absorption. Four hours after ingestion most of the meal has left the stomach and the majority of nutrients have been absorbed. It seems obvious that the stomach must be involved in the termination of eating (satiation). Indeed stomach distension is regarded as being an important satiety signal. A good deal of experimental evidence indicates that gastric distension can arrest eating behavior, but the effect may be short lived. By itself, gastric distension does not appear to produce the sensation of satiety and cannot be the only factor controlling meal size. Indeed, chemicals released by gastric stimuli or by food processing in the gastrointestinal tract are critical to the episodic control of appetite. Many of these chemicals are peptide neuro-transmitters, and many peripherally administered peptides cause changes in food consumption.

There is evidence for an endogenous role for chole-cystokinin (CCK), pancreatic glucagon, gastrin releasing peptide (GRP), and somatostatin. Much recent research has confirmed the status of CCK as a hormone mediating meal termination (satiation) and possibly early phase satiety. Food consumption (mainly protein and fat) stimulates the release of CCK (from duodenal mucosal cells), which in turn activates CCK-A type receptors in the pyloric region of the stomach. This signal is transmitted via afferent fibers of the vagus nerve to the nucleus tractus solitar-ius (NTS) in the brainstem. From here the signal is relayed to the hypothalamic region where integration with other signals occurs. Direct infusions of CCK dose-dependently reduce food intake in mice, rats and monkeys, and in human volunteers the CCK octopeptide CCK-8 reduces food intake and enhances satiety. Peripheral CCK-8 administration has also been shown to increase the release of serotonin in the hypothalamus, a neurotransmitter that has been implicated in the integration of episodic satiety signals.

Other potential peripheral satiety signals include peptides such as enterostatin, neurotensin, and glucagon-like peptide (GLP-1). Researchers are continually searching for components of peripheral metabolism that could provide information to the brain concerning the pattern of eating behavior. There is considerable current interest in the peptide called enterostatin. it is formed by the cleavage of procoli-pase that produces colipase and this 5 amino acid activation peptide. The administration of enterostatin reduces food intake and, since it is increased after high-fat feeding, it has been suggested that enterostatin could be a specific fat-induced satiety signal. Another gut factor stimulated by the ingestion of dietary fat is intestinal glycoprotein apolipoprotein A-iV produced in the human small intestine and released into intestinal lymph in response to dietary lipids.

Glucagon-like peptide 1 (GLP-1) is a hormone that is released from the gut into the bloodstream in response to intestinal carbohydrate. Endogenous GLP-1 levels increase after meals with the largest increase in response to carbohydrate ingestion. in humans, infusions of glucose directly into the gut or the ingestion of carbohydrate produces a decrease in appetite and an increase in blood GLP-1. A series of studies by Meier and coworkers in both lean and obese human volunteers demonstrated that infusions of synthetic human GLP-1 enhanced ratings of fullness and satiety and reduced food intake and spontaneous eating behavior. Recent research has also focused on amylin, a pancreatic hormone, which also has a potent effect on both food intake and body weight. Peripheral administration of amylin reduces food intake in mice and rats, and meal size in rats.

One further source of biological information relevant to the control of appetite concerns fuel metabolism. The products of food digestion may be metabolized in peripheral tissues or organs, or may enter the brain directly. Most research has involved glucose metabolism and fatty acid oxidation in the hepatoportal area. The main hypothesis suggests that satiety is associated with an increase in fuel oxidation. indirect evidence is provided by the use of antimetabolites that block oxidation pathways or impair fuel availability and lead to increases in food intake. it is argued that membranes or tissues sensitive to this metabolic activity modulate afferent discharges that are relayed to the brain via the vagus nerve. Pathways in the CNS that are sensitive to this metabolic signaling have begun to be mapped out. it is difficult to identify CNS mechanisms that specifically integrate short-term satiety signals alone into appetite regulation. Generally, the peripheral release and detection of various gut peptides could account for their satiety function. However, direct entry into, and action on receptors in the CNS, may also contribute to their satiety action. The one central factor clearly associated with episodic satiety, rather than tonic energy status, is serotonin (see below).

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