Appetite centre

The appetite centre in the arcuate nucleus appears to be composed of at least two classes of neurons primary neurons that sense metabohte levels and regulating hormones, and secondary neurons that synchronise information from primary neurons and coordinate bodily functions through vagal signalling. There are those which stimulate appetite through secretion of NPY and the AgRP, and those which depress appetite through secretion of POMC (see also Section 3.9). 

The anorexia suffered by cancer patients is likely to arise from a combination of psychological stress, altered senses of taste and smell and increased levels of cytokines, which influence the appetite and satiety centres in the hypothalamus. There are several consequences micronutrient intake will be diminished and this may contribute to the signs and symptoms of the disease. Plasma amino acid levels will fall, as in starvation (Chapter 16). Synthesis of glutamine (by muscle, adipose and lung), aspartate (by liver), glutathione (by the intestine) and arginine (by the kidney) will all be compromised. The metabolic significance of all of these is discussed in Chapter 18. 

The sequence of alkylation followed by reduction gives an amine and the special advantage of this strategy is that it can lead to r-alkyl amines. The appetite suppressant 15 can be disconnected next to the tertiary centre after the amines are changed to a nitro-compound 16. 2-Nitropropane 18 is available. 

Implementation of self-care and shared-care principles is crucial. Patients should learn about symptoms of DKA and be able to measure ketones in blood or urine. A common lapse is omission/reduc-tion of insulin during episodes with impaired well-being and poor appetite. Persistent ketosis should be treated with extra insulin, fluid and carbohydrate, when necessary. Furthermore, it is very important that the individual patient had ready, 24-h access to diabetological expertise, preferably in a specialised diabetes centre. 

Very rarely, people are overweight or obese as a result of a physical defect of the appetite control centres in the brain — for example, some tumours can cause damage to the satiety centre, so that the patient feels hunger, but not the sensation of satiety, and has no physiological cue to stop eating. 

A number of compounds act either to suppress the activity of the hunger centre in the hypothalamus or to stimulate the satiety centre. Sometimes this is an undesirable side-effect of drugs used to treat disease and can contribute to the undernutrition seen in chronically ill people (section 8.4). As an aid to weight reduction, especially in people who find it difficult to control their food intake, drugs that suppress appetite can be useful. Three compounds are in relatively widespread use as appetite suppressants fenfluramine (and more recently the D-isomer, dexfenfluramine), diethylpropion and mazindol. The combination of phentermine and fenfluramine was withdrawn in the 1990s, after a number of reports associating it with cardiac damage. 

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