There are a number of physiological mechanisms that serve as the basis for hunger. When our stomachs are empty, they contract. Typically, a person then experiences hunger pangs. Chemical messages travel to the brain, and serve as a signal to initiate feeding behavior. When our blood glucose levels drop, the pancreas and liver generate a number of chemical signals that induce hunger (Konturek et al., 2003; Novin, Robinson, Culbreth, & Tordoff, 1985) and thus initiate feeding behavior.
For most people, once they have eaten, they feel satiation, or fullness and satisfaction, and their eating behavior stops. Like the initiation of eating, satiation is also regulated by several physiological mechanisms. As blood glucose levels increase, the pancreas and liver send signals to shut off hunger and eating (Drazen & Woods, 2003; Druce, Small, & Bloom, 2004; Greary, 1990). The food’s passage through the gastrointestinal tract also provides important satiety signals to the brain (Woods, 2004), and fat cells release leptin, a satiety hormone.
The various hunger and satiety signals that are involved in the regulation of eating are integrated in the brain. Research suggests that several areas of the hypothalamus and hindbrain are especially important sites where this integration occurs (Ahima & Antwi, 2008; Woods & D’Alessio, 2008). Ultimately, activity in the brain determines whether or not we engage in feeding behavior (Figure 10.9).
The content of this course has been taken from the free Psychology textbook by Openstax