Food intake is the result of feeling hungry; a feeling of hunger initiates due to a decline in blood glucose level. This decline in blood glucose level is sensed by specialized cells that are located in the hunger centre of the brain. The hunger centre is present in the hypothalamus region of the brain (in the lateral hypothalamic area or LHA). This centre stimulates food intake/feeding after a person feels hungry. On the other hand, food intake/feeding results in a rising blood glucose level that stimulates the satiety centre of the hypothalamus (in ventral medial hypothalamus or VHM). VHM inhibits the activity of LHA that terminates the feeding/food intake.
However, some scientific studies have shown that initiation of hunger is a complex process and occurs as a result of many different factors, neural and endocrine processes. Blood glucose levels can control hunger or appetite only if a person is severely low in energy (energy-deprived). Other factors like cultural, social, and psychological also play a role in food intake. They can either cause increased food intake (known as hyperphagia) or decreased food intake (hypophagia). Nevertheless, the hypothalamus plays a key role in the regulation of food intake by controlling appetite.
Hypothalamus receives two types of signals/inputs –
Orexigenic: These signals stimulate appetite/hunger.
Anorexigenic: These signals inhibit appetite/hunger.
Further, these signals can be peripheral or central, depending on their location where they originate in the nervous system.
Arcuate nucleus
The arcuate nucleus is a structure formed by a collection of neurons in the hypothalamus. The arcuate nucleus plays an important role in food intake regulation. It produces orexigenic and anorexigenic substances that act as respective signals. One such substance is a neuropeptide Y (NPY) that acts as an orexigenic signal. This signal reaches the lateral hypothalamic area or LHA. As a result, LHA releases a hormone called MCH (Melanin Concentrating Hormone), which also acts as an orexigenic signal. Both of these signals are generated in absence of enough inhibition signals or under the influence of social/cultural/psychological factors. These signals initiate food intake by initiating hunger.
Proopiomelanocortin (POMC) is one of the anorexigenic substances produced by the arcuate nucleus. It acts as an important anorexigenic signal. Other examples of anorexigenic substances include oxytocin, corticoliberin (CRH), and thyrotropic hormone (TRH). norexigenic signals inhibit feeding/hunger.
Satiety signals
Satiety signals are the different substances produced in the gastrointestinal tract/GI tract that helps in feeding regulation. They can be considered as peripheral anorexigenic substances or signals. These signals are responsible for the termination of feeding/food intake by generating the satiety feeling. Satiety is a feeling of fullness/satisfaction after food intake. These signals are generated within the GI tract as the food moves through the GI tract. GI tract is connected to ANS (Autonomic Nervous System) through its nerve fibre endings or axons. These signals stimulate ANS through connected nerve fibres. The nerve fibres from ANS end in a structure called solitary tract nuclei in the brain stem. GI tract sends satiety signals to brain stem, which in turn passes the information to the satiety centre of the hypothalamus that inhibits feeding/food intake.
Examples of satiety signals include CCK (cholecystokinin), GLP-1 (glucagon-like peptide-I), amylin, somatostatin, bombesin, entertain, and others.
GI tract can also produce an orexigenic signal. For example – Ghrelin (which is the only GI peptide) acts as an orexigenic signal. It stimulates the intake of large food portions.
Adiposity signals also play a role in achieving satiety. One such signal is leptin, which is released by adipose tissue. Its main role is metabolism, but it also plays a signaling role. If the level of leptin is higher, then it stimulates POMC release (anorexigenic signal) to produce a feeling of satiety. If its level is lower, then it stimulates Y (NPY) release (orexigenic signal) that produces a feeling of hunger. However, anorexigenic effect of leptin is stronger than orexigenic effect. Insulin is another substance that acts as adiposity signal. The pancreas secretes it. It has a strong anorexigenic effect that inhibits food intake and produces satiety feeling by stimulating POMC release.
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