CONTROL SIGNALS
The following descriptions of the different signals that control appetite are placed roughly in the order in which they are activated during a meal. All of these signals must be integrated by the brain.
1 Sensory-specific satiety
The following descriptions of the different signals that control appetite are placed roughly in the order in which they are activated during a meal. All of these signals must be integrated by the brain.
1 Sensory-specific satiety
If we eat as much of one food as we want, the pleasantness rating of its taste and smell change from very pleasant to neutral. But other foods may still taste and smell pleasant. So variety stimulates food intake.
For example, if you eat as much chicken as you want for a meal, the pleasantness rating of the taste of chicken decreases to roughly neutral. Bananas, on the other hand, may remain pleasant, so you might eat them as a second course even when the chicken has already ‘filled you up’, or produced satiety. This type of satiety is partly specific to the sensory qualities of the food, including its taste, smell, texture and appearance, and has therefore been named sensory-specific satiety (Rolls, 1999).
2 Gastric distension
Normally gastric distension is one of the signals necessary for satiety. As we saw earlier, this is demonstrated when gastric drainage of food after a meal leads to immediate resumption of eating.
Gastric distension only builds up if the pyloric sphincter closes. [pyloric sphincter controls the release of food from the stomach to the duodenum] The pyloric sphincter controls the emptying of the stomach into the next part of the gastrointestinal tract, the duodenum. The sphincter closes only when food reaches the duodenum, stimulating chemosensors [chemosensors receptors for chemical signals such as glucose concentration] and osmosensors [osmosensors receptors for osmotic signals] to regulate the action of the sphincter, by both local neural circuits and hormones.
3 Duodenal chemosensors
The duodenum contains receptors sensitive to the chemical composition of the food draining from the stomach. One set of receptors respond to glucose and can contribute to satiety via the vagus nerve, which carries signals to the brain. The vagus is known to represent the critical pathway because cutting this nerve (vagotomy) abolishes the satiating effects of glucose infusions into the duodenum. Fats infused into the duodenum can also produce satiety, but in this case the link to the brain may be hormonal rather than neural (a hormone is a blood-borne signal), since vagotomy does not abolish the satiating effect of fat infusions into the duodenum (see Greenberg, Smith & Gibbs, 1990; Mei, 1993).
4 Glucostatic hypothesis
We eat in order to maintain glucostasis – that is, to keep our internal glucose level constant. Strictly, the crucial signal is the utilization of glucose by our body and brain, as measured by the difference between the arterial and the venous concentrations of glucose. If glucose utilization is low, indicating that the body is not able to extract much glucose from the blood stream, we feel hungry, whereas if utilization is high, we feel satiated. This is confirmed by the following findings:
Rats show a small decrease in plasma glucose concentration just before meals, suggesting that decreased glucose concentration initiates eating (Campfield & Smith, 1990) . At the end of a meal, plasma glucose concentration rises, and so does insulin, which helps the glucose to be used by cells.
Injections of insulin, which reduce the concentration of glucose in the plasma ( by facilitating its entry to cells and storage as fat), provoke food intake.
Infusions, or injections, of glucose and insulin (together enabling glucose to be taken up by the body’s cells) can reduce feeding.
The brain’s monitoring system for glucose availability seems to be in the part of the brain called the medulla ( part of the brainstem), because infusions there of a competitive inhibitor of glucose (5-thio-glucose) also provoke feeding (Levin et al., 2000).
5 Body fat regulation and the role of leptin
For example, if you eat as much chicken as you want for a meal, the pleasantness rating of the taste of chicken decreases to roughly neutral. Bananas, on the other hand, may remain pleasant, so you might eat them as a second course even when the chicken has already ‘filled you up’, or produced satiety. This type of satiety is partly specific to the sensory qualities of the food, including its taste, smell, texture and appearance, and has therefore been named sensory-specific satiety (Rolls, 1999).
2 Gastric distension
Normally gastric distension is one of the signals necessary for satiety. As we saw earlier, this is demonstrated when gastric drainage of food after a meal leads to immediate resumption of eating.
Gastric distension only builds up if the pyloric sphincter closes. [pyloric sphincter controls the release of food from the stomach to the duodenum] The pyloric sphincter controls the emptying of the stomach into the next part of the gastrointestinal tract, the duodenum. The sphincter closes only when food reaches the duodenum, stimulating chemosensors [chemosensors receptors for chemical signals such as glucose concentration] and osmosensors [osmosensors receptors for osmotic signals] to regulate the action of the sphincter, by both local neural circuits and hormones.
3 Duodenal chemosensors
The duodenum contains receptors sensitive to the chemical composition of the food draining from the stomach. One set of receptors respond to glucose and can contribute to satiety via the vagus nerve, which carries signals to the brain. The vagus is known to represent the critical pathway because cutting this nerve (vagotomy) abolishes the satiating effects of glucose infusions into the duodenum. Fats infused into the duodenum can also produce satiety, but in this case the link to the brain may be hormonal rather than neural (a hormone is a blood-borne signal), since vagotomy does not abolish the satiating effect of fat infusions into the duodenum (see Greenberg, Smith & Gibbs, 1990; Mei, 1993).
4 Glucostatic hypothesis
We eat in order to maintain glucostasis – that is, to keep our internal glucose level constant. Strictly, the crucial signal is the utilization of glucose by our body and brain, as measured by the difference between the arterial and the venous concentrations of glucose. If glucose utilization is low, indicating that the body is not able to extract much glucose from the blood stream, we feel hungry, whereas if utilization is high, we feel satiated. This is confirmed by the following findings:
Rats show a small decrease in plasma glucose concentration just before meals, suggesting that decreased glucose concentration initiates eating (Campfield & Smith, 1990) . At the end of a meal, plasma glucose concentration rises, and so does insulin, which helps the glucose to be used by cells.
Injections of insulin, which reduce the concentration of glucose in the plasma ( by facilitating its entry to cells and storage as fat), provoke food intake.
Infusions, or injections, of glucose and insulin (together enabling glucose to be taken up by the body’s cells) can reduce feeding.
The brain’s monitoring system for glucose availability seems to be in the part of the brain called the medulla ( part of the brainstem), because infusions there of a competitive inhibitor of glucose (5-thio-glucose) also provoke feeding (Levin et al., 2000).
5 Body fat regulation and the role of leptin
The signals described so far help to regulate hunger from meal to meal, but they are not really adequate for the long-term regulation of body weight and, in particular, body fat. So the search has been on for scientists to identify another signal that might regulate appetite, based on, for example, the amount of fat in the body. Recent research has uncovered a hormone, leptin (also called OB protein), which performs this function (see Campfield et al., 1995).
6 Conditioned appetite and satiety
6 Conditioned appetite and satiety
If we eat food containing lots of energy (e.g. rich in fat) for a few days, we gradually eat less of it. If we eat food with little energy, we gradually, over days, ingest more of it. This regulation involves learning to associate the sight, taste, smell and texture of the food with the energy that is released from it in the hours after it is eaten. This form of learning has been demonstrated by Booth (1985).
Two groups of participants ate different flavoured sandwiches – one flavour being high energy sandwiches and the other being low energy. On the critical test day, the participants chose to eat few of the sandwiches that tasted like the high energy ones eaten previously, but far more of the sandwiches that had the flavour of the previously consumed low energy sandwiches. And yet, on the test day, all the sandwiches consumed in fact had medium energy content. This suggests that the level of consumption of the medium energy sandwiches on the test day was strongly influenced by the energy content of the sandwiches that had been eaten previously.
Two groups of participants ate different flavoured sandwiches – one flavour being high energy sandwiches and the other being low energy. On the critical test day, the participants chose to eat few of the sandwiches that tasted like the high energy ones eaten previously, but far more of the sandwiches that had the flavour of the previously consumed low energy sandwiches. And yet, on the test day, all the sandwiches consumed in fact had medium energy content. This suggests that the level of consumption of the medium energy sandwiches on the test day was strongly influenced by the energy content of the sandwiches that had been eaten previously.
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