As shown in Figure 1.3, there are hunger and satiety centres in the brain, which stimulate us to begin eating (the hunger centres in the lateral hypothalamus) and to to stop eating when hunger has been satisfied (the satiety centres in the ventromedial hypothalamus). A great deal is known about the role of these brain centres in controlling food intake, and there are a number of drugs which modify responses to hunger and satiety. Such drugs can be used to reduce appetite in the treatment of obesity (section 6.3.3) or to stimulate it in people with loss of appetite or anorexia.
What is not known is what signals hunger or satiety to these hypothalamic centres. It may be the relative concentrations of glucose, triacylglycerols, non-esterified fatty acids and ketone bodies available as metabolic fuels in the fed and fasting states (section 5.3). Equally, the relative concentrations of the hormones insulin and glucagon (section 5.3 and section 10.5) and some of the peptide hormones secreted by the gastrointestinal tract during digestion of food may be important. There is also evidence that the amount of the amino acid tryptophan available for uptake into the brain may be important; tryptophan availability to the brain is controlled by both the concentration of tryptophan relative to other large neutral amino acids (section 4.4.1) and the extent
Amygdala (temporal lobe) - learned food behaviour
to which it is bound to serum albumin — non-esterified fatty acids displace tryptophan from albumin binding, making it more readily available for brain uptake.
There is experimental evidence that the liver may play a key role in controlling appetite. In the fasting state there is a considerable increase in citric acid cycle activity in the liver (section 5.4.4) as the liver metabolizes fatty acids and other fuels to provide the adenosine triphosphate (ATP) required for synthesis of glucose from amino acids and other non-carbohydrate precursors (the process of gluconeogenesis; section 5.7) in order to maintain the plasma concentration of glucose. This hepatic 'energy flow' hypothesis still begs the question of what provides the signal from the liver to the central nervous system; although there are sensory neuronal pathways from the liver, lesioning them does not affect feeding behaviour in experimental animals.
The hypothalamic hunger and satiety centres control food intake remarkably precisely. Without conscious effort, most people can regulate their food intake to match energy expenditure very closely — they neither waste away from lack of metabolic fuel for physical activity nor lay down excessively large reserves of fat. Even people who have excessive reserves of body fat and can be considered to be so overweight or obese as to be putting their health at risk (section 6.2.2) balance their energy intake and expenditure relatively well considering that the average intake is a tonne of food a year, whereas the record obese people weigh about 250 kg (compared with average weights between 60 and 100 kg), and it takes many years to achieve such a weight. A gain or loss of 5 kg body weight over 6 months would require only a 1% difference between food intake and energy expenditure per day (section 5.2).
Was this article helpful?