Metabolic aspects of satiety

The simple view of satiety is that it occurs when the combined strength of signals from gastrointestinal and liver receptors reaches a threshold.However, this does not allow for long-term balancing of feed intake with requirements, as in order to match food intake with requirements feeding must terminate long before the animal knows how much of the various nutrients have been absorbed.Therefore, some way(s) of predicting nutrient availability is required.Learned associations between the organoleptic properties of a food and its eventual nutritive values is one mechanism.Another is the learned association between the gastrointestinal effects and eventual yield of nutrients, while another is learned associations between the early metabolic effects of the nutrients absorbed from a meal on liver and brain, and eventual nutrient yield.It is not anticipated that the total of all these mechanisms could be accurate, so that feedbacks from the regulated stores of nutrients are required in addition to the previously mentioned immediate effects of a meal on feeding.Therefore, satiety is induced and feeding ceases at a point at which the total of all the signals, from both direct physical and chemical stimuli and from learned associations, reach a satiating level.It is the purpose of the present review to consider the components of this complex that are generated within the body directly and indirectly as a result of eating.In searching for satiety signals we are looking for changes in the body that go in one direction during a meal, may continue in that direction for some time after the meal, but eventually return to the premeal level.There are many metabolites and hormones which exhibit such changes and several will be examined in turn, some more cursorily than others in view of the brevity of the present review. GLUCOSEOne of the original 'metabolic' theories of intake control postulated that animals eat in order to maintain a relative constancy of blood glucose concentration and the classical glucostatic theory of food intake control envisages central nervous sensitivity to glucose.While this has since been broadened to encompass energy utilization or availability, the fact that glucose is the major source of energy in many animals has meant that it continues to be viewed as a major contributor to satiety.Plasma glucose rises during a meal and peaks shortly after the meal ends (Louis-Sylvestre & Le Magnen, 1980) and could be a direct cause of satiation.Preventing the fall in blood glucose concentration which normally occurs just before a meal, in rats, maintained satiety so that animals which would have otherwise started to eat 12 min later actually waited 318 min before starting to eat (Campfield et al. 1985).Glucose introduced into the stomach has a much greater effect on the size of a subsequent meal than the same amount of the unabsorbable analogue of glucose, 3-0-methylglucose (Booth, 1972a), showing that the metabolic effect of glucose is more important than the osmotic effect; fructose, which is used by the liver, was as effective as glucose in suppressing