Body weight is often considered to be the result of energy intake and energy expenditure. These two factors vary dramatically between individuals, yet in the general population we do not see the huge variance in body weight that would reflect this. Therefore it is assumed that there is a physiological mechanism that contributes to the steady control of body weight and composition.
The hypothalamus is known to play an important role in appetite and weight regulation. Studies done in the 20th century have shown that damage to the hypothalamic nuclei can cause hyperphagia (overeating) in rodents. The ventromedial nucleus (VMN) is thought to control satiety and is known as the satiety centre. The dorsomedial nucleus (DMN) or the paraventricular nucleus (PVN) also contribute to energy balance as damage to either area results in increased food intake and weight gain. The lateral hypothalamic area (LHA) is known as the 'feeding centre' as damage to this area results in reduced food intake and weight loss.
How energy balance is achieved depends on signals received from the periphery via the blood. Many studies now focus on particular peptides secreted from the hypothalamus that act as messengers in controlling the body's energy stores. Information on nutrient stores, satiety, hunger and taste are fed back to the brain where it is interpreted and causes the release of the appropriate neuropeptides and transmitters.
Neurotransmitters and neuropeptides implicated in feeding stimulation (orexigenic) or inhibition (anorexigenic) are shown below.
There is strong evidence for a role for neuropeptide Y (NPY) in feeding. Although it is abundant in all parts of the brain, it is especially concentrated in the hypothalamus. Injection of this mediator into the rodent brain causes an increase in food intake, especially if injected into the PVN. Chronic administration of NPY leads to hyperphagia, decreased thermogeneis and obesity. Injection of an antibody to NPY can decrease the above affect.
While NPY has an important role in body weight, there are other mediators that are also important. Removing the gene responsible for producing NPY in mice leads to normal feeding behaviour and body weight. However in mice where both NPY and leptin are deficient the result is decreased obesity with reduced food intake and increased energy expenditure.