The Physiological Mechanisms That Influence Food Intake Food intake is a rather complex physiological process which can be affected by the information coming from the digestive tract, nutrients availability or deficit reported by body cells, and should also be analysed and interpreted by the nervous system. Thus, there are a number of mechanisms and factors which affect the feeling of satiety and hunger.
The direct role of hypothalamus in control of appetite is provided by neurons sensitive to
changes in glucose concentration. They monitor extracellular blood glucose levels and respond in two different manners: increase in firing rate for glucose excited (GE) neurons or decrease in firing rate for glucose inhibited (GI) ones (O’Malley et al., 2007). In the result of sensing of high glucose levels, the feeling of satiety develops (Ahima and Antwi, 2009). However, when the blood glucose drops, hypothalamus initiates the feeling of hunger and search for food. Orexin, also known as hypocretin, is a hormone produced by the latheral hypothalamus which also contributed to increased food intake. The neurons secreting this hormone are activated by decreased blood glucose and by stomach hormone ghrelin (Bartness et al., 2011). In order to avoid the increased amount of food intake, hypothalamus should have a feedback about the filling of the stomach. Such feedback is provided by the vagus nerve, carrying information from the mechanoreceptors in the stomach to the dorsal vagal complex in medulla, and terminating on the neurons of the nucleus of solitary tract (NTS). Projections from NTS then innervate certain areas of hypothalamus responsible of feeling of satiety (Ahima and Antwi, 2009).
At the same time, the central melanocortin system affects the functioning of hypothalamus and interpretation of information it receives. In turn, the system can be affected by a number of molecules which come from other brain regions as well as from the peripheral tissues. The central melanocortin system consists of neurons producing melanocortins and neurons within the hypothalamus arcuate nucleus expressing the corresponding receptors.
Neurons which respond to melanocrotin produce proopiomelanocortin (POMC), neuropeptide Y (NPY) and agoutirelated peptide (AgRP). POMC neurons release the anorexigenic peptides while the other two types of neurons release the orexigenic ones. Release of melanocortin leads
to reduced appetite and food intake. This effect is explained by activation of the POMC neurons and inhibition of the NPY and AgRP neurons (Xu et al. 2012). NPY is associated with increased food intake under the decreased temperatures. It contributes to increased adipogenesis and reduced lipolysis (Xu et al. 2012). CRH is produced by POMC neurons of hypothalamus and contributes to release of adrenocorticotropic hormone, stimulating the production of glucocorticoids (George et al., 2011). They were shown to inhibit the POMC, and to activate NPY and AgRP producing neurons, decreasing the food intake and leading to weight loss (Kim et al., 2014).
At the same time, a number of molecules produced by the peripheral tissues also affect
the functioning of the central melanocrotin system and thus, hypothalamus. Insulin, widely
known as a hormone regulating blood glucose, also has receptors in different regions of brain. It was shown that insulin can decrease the appetite via binding to its receptors on POMC neurons (Kim et al., 2014). Leptin is the other molecule which reduces the appetite. It is produced by the adipose tissue in the amount proportional to the body fat. When the amount of adipose tissue is high, the levels of leptin are also high and it binds to leptin receptors on POMC and NPY neurons, activating the first one and inhibiting the last one. Thus, appetite is reduced when body fat increases. At the same time, low amount of adipose tissue leads to low levels of leptin in blood, and thus, reduced activity of anorexigenic POMC neurons and increased activity of NPY neurons (Kim et al., 2014). There are also two hormones produced by the gastrointestinal system, which provide the humoral feedback about stomach filling. Ghrelin is a hormone produced by specialized cells of the stomach when it is empty. It contributes to increased food intake via inhibiting the POMC neurons and activating the NPY/AgRP ones. Peptide YY (PYY) is produced by the intestinal cells in response to nutrients income. Close location of vagal afferents to the cells producing PYY allows the hormone to affect vagus, which passes the signals about
satiety to the central nervous system. In addition, it was shown that PYY inhibits the activity of NPY neurons (Côté et al., 2014).
Therefore, hypothalamus is the central coordinator of food intake, the functioning of
which can be affected by the central melanocortin system, used for the perception of body
signals coming from peripheral tissues as well as for the coordination of the functioning of
hypothalamus with the other parts of brain.
References
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