Scientifically important components of the appetite system are those physiological events which are triggered as responses to the ingestion of food and which form the inhibitory processes that first of all stop eating and then prevent the re-occurrence of eating until another meal is triggered. These physiological responses are termed satiety signals, and can be represented by the satiety cascade (Figure 8.2).
Satiation can be regarded as the complex of processes which brings eating to a halt (cause meal termination) whilst satiety can be regarded as those events which arise from food consumption and which serve to suppress hunger (the urge to eat) and maintain an inhibition over eating for a particular
period of time. This characteristic form of an eating pattern (size of meals, snacks etc.) is therefore dependent upon the coordinated effects of satiation and satiety which control the size and frequency of eating episodes.
Initially the brain is informed about the amount of food ingested and its nutrient content via sensory input. The gastrointestinal tract is equipped with specialized chemo- and mechano-receptors that monitor physiological activity and pass information to the brain mainly via the vagus nerve (4). This afferent information constitutes one class of 'satiety signals' and forms part of the pre-absorptive control of appetite. It is usual to identify a post-absorptive phase that arises when nutrients have undergone digestion and have crossed the intestinal wall to enter the circulation. These products, which accurately reflect the food consumed, may be metabolized in the peripheral tissues or organs or may enter the brain directly via the circulation. In either case, these products constitute a further class of metabolic satiety signals. Additionally, products of digestion and agents responsible for their metabolism may reach the brain and bind to specific chemoreceptors, influence neurotransmitter synthesis or alter some aspect of neuronal metabolism. In each case the brain is informed about some aspects of the metabolic state resulting from food consumption.
It seems likely that chemicals released by gastric stimuli or by food processing in the gastrointestinal tract are involved in the control of appetite (5). Many of these chemicals are peptide neurotrans-mitters, and many peripherally administered pept-ides cause changes in food consumption (6). There is evidence for an endogenous role for cholecystokinin (CCK), pancreatic glucagon, bombesin and somatostatin. Much recent research has confirmed the status of CCK as a hormone mediating meal termination (satiation) and possibly early phase satiety. This can be demonstrated by administering CCK intravenously (the mouth cannot be used since CCK would be inactivated as soon as it reached the stomach) and measuring changes in food intake and hunger. CCK will reduce meal size and also suppress hunger before the meal; these effects do not depend on the nausea that sometimes accompanies an intravenous infusion (7). 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 fibres of the vagus nerve to the nucleus tractus solitarius (NTS) in the brainstem. From here the signal is relayed to the hypothalamic region where integration with other signals occurs. The components of this system are set out in Figure 8.3.
Other potential peripheral satiety signals include peptides such as enterostatin (8), neurotensin and glucagon-like peptide 1 (GLP-1) (9).
Was this article helpful?
Many women who have recently given birth are always interested in attempting to lose some of that extra weight that traditionally accompanies having a baby. What many of these women do not entirely realize is the fact that breast-feeding can not only help provide the baby with essential vitamins and nutrients, but can also help in the weight-loss process.