Biological Mechanisms of Hunger What Causes Hunger:

Biological Mechanisms of Hunger

What Causes Hunger: The Biological Mechanisms of Hunger

The biological mechanisms that trigger hunger are rather complex. In that regard, several theories have been proposed in an attempt to explain hunger and the biological mechanisms that control it. It is therefore important to note that the feeling of hunger has no single source. Indeed, as Pastorino and Doyle-Portillo (2012) point out; although the stomach plays a role in the initiation of hunger, it is not the only source of the same.

The liver according to Pastorino and Doyle-Portillo (2012) plays an important part in the regulation of hunger. This it accomplishes by closely monitoring not on the levels of glucose but also the levels of glycogen in the body. In basic terms, glucose (a form of sugar) is burnt by our bodies for energy. On the other hand, glycogen according to Pastorino and Doyle-Portillo (2012) "is the form of starch that we store along with fatty acids." Glucose deemed by the body to be in excess of the required amount is converted into glycogen and stored for future utilization (Pastorino and Doyle-Portillo, 2012). As the authors further point out, the liver from time to time monitors our glucose and glycogen levels so as to determine our energy requirements. In this case the conversion of glucose into glycogen is often an indicator that our bodies have too much fuel. In such a case, the liver sends "signals to the brain to shut off hunger" (Pastorino and Doyle-Portillo, 2012). The authors on the other hand point out that when the liver finds out that we are eating into our energy reserves (as a result of the reconversion of glycogen to glucose); it signals the brain to trigger a hunger feeling.

It is also important to note that feelings of hunger can also be triggered by insulin. Insulin according to Pastorino and Doyle-Portillo (2012) is charged with the facilitation of "the movement of glucose from the blood into our cells, where it is metabolized." In that regard, the movement of glucose into the cells triggers a decline in the level of glucose in the blood. Hunger is initiated when the body starts using up the glycogen reserves.

According to Pastorino and Doyle-Portillo (2012), when it comes to our eating behavior, the brain also does play an important role. As the authors point out, in addition to receiving and processing contraction and distention signals form the stomach, the brain also acts upon signals received from the liver regarding the levels of glucose and glycogen.

The glucostatic theory of hunger according to Wagner (2004) was proposed by Mayer. According to the author, this theory postulates that when the level of glucose in the blood drops below a set point, this acts as a signal for eating to commence. Eating stops when the blood glucose level rises to the set point again (Wagner, 2004). However, when it comes to the dual-center set-point model, Wagner (2004) in his own words points out that "eating commences with the stimulation of the LH feeding center by decreasing blood glucose, and ceases with the stimulation of VMH satiety center by blood glucose above the set point." It should be noted that the glucostatic theory has more evidence to support it than the dual-center set-point model which according to Wagner () has been rejected for several reasons. In regard to the glucostatic theory, the brain's glucoreceptors are said to be the sensors of the level of glucose in the blood. According to Wagner (2004), when these glucoreceptors are destroyed in rats, the affected animals start overeating.