Appetite satiety

Galanin Present in secretomotor neurons may play a role in appetite-satiety mechanisms. 

Whilst only 4% of the UK diet is fibre, there are few parts of the process of digestion and absorption which fibre does not influence to some extent. Experimental evidence exists to show that appetite, satiety, gastric emptying, carbohydrate, sterol and mineral absorption may all be affected by fibre. 

Cholecystokinin (CCK) is produced in the intestine and the brain. It appears to be an important mediator of anxiety. It also stimulates vasopressin secretion and slows gastric emptying. In addition, it is an important humoral satiety signal (appetite control). Various antagonists have been developed and are currently being investigated with regard to their therapeutic potential. 

Sibutramine and its two active metabolites (Mj and M2) exert their effect by inhibiting the reuptake of serotonin, norepinephrine, and dopamine.29 Appetite becomes suppressed because patients feel a sense of satiety. 

Figure 3.1 Appetite is controlled by many body processes, as shown here. The arrows indicate things that increase and decrease hunger. All of these processes work by sending signals to the brain to indicate a feeling of hunger or satiety (fullness). Certain diet pills called appetite suppressants may work in the same way as some of these body processes, by sending signals to the brain that indicate satiety and say stop eating ...

Appetite Stimulants. A large body of neuroscience research indicates that serotonin plays a prominent role in the modulation of appetite. Increases in serotonin availability in certain brain regions confer a sense of satiety, and decreases of serotonin are associated with hunger. Consequently, agents that block the release or action of serotonin in the brain increase appetite and should theoretically be helpful in the treatment of AN. 

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. 

Peptide YY (PYY) is a peptide hormone produced by L-cells in the intestinal tract after eating. It appears to act centrally to diminish appetite. It may serve normally to produce a sense of satiety. Diminished PYY production would be expected to cause increase in appetite and increased food intake. Hence, a biologically active PYY derivative, PYY 3-36, is under investigation as a potential agent to treat obesity and type 2 diabetes. A nasal PYY 3-36 product, if developed, would be an attractive alternative to injected PYY 3-36 because of the rapid and direct nose-to-brain drug transport that occurs following nasal drug delivery. 

Of special interest in the control of obesity are factors that regulate appetite and satiety. 

Drugs for obesity act either on the gastrointestinal tract to lower nutrient absorption or centrally to reduce food intake by decreasing appetite or increasing satiety (appetite suppressants). 

CCK acts on the brain to control the appetite. Most studies involving CCK and eating behavior show that increases in the plasma levels of CCK are closely associated with satiety. CCK is concentrated in specific regions m the brain, where it acts locally. The term locally in this instance means that the hormone is produced by the brain and acts only in the brain. Further details on appetite physiology appear in the Obesity chapter. 

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