Neural and hormonal mechanisms involved in the control of eating behaviour
Neural mechanisms concern the influence of brain components in regulating eating behaviour. The dual control theory is based on the idea of a homeostatic perception of hunger and satiety (fullness), whereby when the level of glucose (blood sugar) is low, the liver sends signals to the lateral hypothalamus, creating a sensation of hunger that motivates an individual to eat. When food is eaten, glucose is released, activating the ventromedial hypothalamus (VMH), producing a sensation of satiety, which stops further eating. Alternatively set-point theory (SPT) suggests everyone has a ’set-point’ weight their body is shaped towards, determined by the rate at which calories are consumed. Set-points alter depending on several factors, including eating patterns and exercise. Hormonal mechanisms are chemical messengers within the body that influence eating behaviour. Leptin is a hormone produced by fat cells which signals to the hypothalamus that calorific storage is low and so is associated with decreasing appetite. Ghrelin is a hormone secreted from the lining of the stomach, whose concentration in the blood falls after eating and rises until the next. Ghrelin signals to the hypothalamus to increase the sensation of hunger and stimulates eating. As leptin also helps stimulate hunger, it may be that leptin helps regulate ghrelin levels.
Fig 13.2 The hypothalmic nuclei involved in the regulation of appetite
Nakazato et al. (2001) assessed the role of the hormone ghrelin in eating behaviour, especially its involvement with the stimulation of appetite and feeding. Injections of ghrelin were given to normal rats and to rats bred to be genetically deficient in growth hormone. It was found that the injections strongly stimulated feeding in the normal rats, leading to significant increases in body weight. Feeding also increased in the genetically deficient rats. Subsequently, injections of anti-ghrelin immunoglobulin G robustly suppressed feeding behaviour in both groups of rats. This illustrated the important role that ghrelin plays in promoting eating and releasing growth hormone. As ghrelin was also seen to influence NPY gene expression and to decrease the influence of the hormone leptin (which is known for its role in decreasing appetite) the findings additionally suggest that there is a competitive interaction between ghrelin and leptin.
• Teitelbaum (1957) got rats to push a bar an increasing number of times to get food. Lesioned VMH rats initially work hard in line with dual control theory (DCT), but work less hard as more presses are required. VMH lesioned rats were also fussy eaters and ate less than normal rats if food tasted stale or bitter. These findings do not support DCT.
• Powley & Keesey (1970) found rats that lose weight through starvation and then have lesions made to their LH do not lose further weight, supporting SPT as it indicates that the rats had slimmed down to a new set-point before the lesions were created.
• Baicy et al. (2007) found that leptin binds to NPY neurons in the arcuate nucleus brain area, decreasing the activity of these neurons, which signals to the hypothalamus to produce a sensation of satiety. This illustrates the key role leptin plays in controlling eating.
Dual control theory does not have universal research support, while set-point theory has a wealth of evidence to back it up, which suggests that set-point theory is a more valid explanation of eating behaviour.
Much research into neural mechanisms has involved animal experimentation, which creates problems in generalising findings to humans. However, Quaade (1971) found that stimulating the ventromedial hypothalamus in obese people made them hungry, and findings from post-mortem studies also back up those from animal studies, which suggests that results of animal studies are therefore generalisable to humans.
Perceiving the lateral hypothalamus (LH) as a ’feeding centre’ is oversimplified, as it is possible to recover from LH lesions and LH lesions also produce disruptions in aggression levels, sexual behaviour and reinforcement behaviour.
The various signals sending information to the hypothalamus are only part of the complex systems regulating eating, as other factors apart from neural mechanisms play a role too, like biological rhythms.
Although hypothalamic mechanisms are important in controlling hunger and satiety, they’re not fully understood. For example, it is not clear how ghrelin and leptin reach targets in the brain, as both are large peptides that do not cross the blood—brain barrier readily.
As leptin is seen to reduce appetite, leptin therapy was devised to treat obesity. However, although leptin injections reduce weight in some obese people, it is not universally effective. Current thinking is that leptin therapy may be more helpful in preventing weight regain than in achieving weight loss.