Signals for Hunger and Satiety

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Chapter 8 Motivation and Emotion
Eating
䉴 What makes me start eating and stop eating?
At first glance, eating seems to be a simple example of drive reduction theory at work.
You get hungry when you haven’t eaten for a while. Much as a car needs gasoline, you
need fuel from food, so you eat. But what bodily mechanism acts as a “gauge” to signal the need for fuel? What determines which foods you eat, and how do you know
when to stop? The answers to these questions involve complex interactions between the
brain and the rest of the body (Hill & Peters, 1998).
Signals for Hunger and Satiety
A variety of mechanisms underlie hunger, the general state of wanting to eat, and satiety (pronounced “seh-TYE-eh-tee”), the general state of no longer wanting to eat.
The stomach would seem to be a logical source of signals for hunger and satiety. You have probably felt “hunger pangs” from an “empty”
stomach and felt “stuffed” after overeating. In fact, the stomach does contract during
hunger pangs, and increased pressure within the stomach can reduce appetite (Cannon &
Washburn, 1912; Houpt, 1994). But people who have lost their stomachs due to illness
still get hungry, and they still eat normal amounts of food (Janowitz, 1967). So stomach cues can affect eating, but they appear to operate mainly when you are very hungry or very full.
Signals from the Stomach
The most important signals about the body’s fuel level
and nutrient needs are sent to the brain from the blood. The brain’s ability to “read”
blood-borne signals about the body’s nutritional needs was discovered when researchers
deprived rats of food for a long period and then injected some of the rats with blood
from rats that had just eaten. When offered food, the injected rats ate little or nothing
(Davis et al., 1969). Something in the injected blood of the well-fed animals apparently
signaled the hungry rats’ brains that there was no need to eat. What was that satiety
signal? Research has shown that the brain constantly monitors both the level of food
nutrients absorbed into the bloodstream from the stomach and the level of hormones
released into the blood in response to those nutrients (Korner & Leibel, 2003).
The nutrients that the brain monitors include glucose (the main form of sugar used
by body cells), fatty acids (from fat), and amino acids (from protein). When the level
of blood glucose drops, eating increases sharply (Mogenson, 1976). The brain also monitors hormone levels to regulate hunger and satiety. For example, when glucose levels
rise, the pancreas releases insulin, a hormone that most body cells need in order to use
the glucose they receive. Insulin itself may also provide a satiety signal by acting directly
on brain cells (Brüning et al., 2000; Schwartz et al., 2000).
The hormone leptin (from the Greek word for “thin”) also appears to provide a satiety signal to the brain (Farooqi et al., 2001; Margetic et al., 2002). Unlike glucose and
insulin, whose satiety signals help us know when to end a particular meal, leptin
appears to be involved mainly in the long-term regulation of body fat (Huang & Li,
2000). The process works like this: Cells that store fat normally have genes that produce leptin. As the fat supply in these cells increases, leptin is released into the blood,
helping to reduce food intake. Animals with defects in these genes make no leptin and
are obese (Bouret, Draper, & Simerly, 2004). When these animals are given leptin injections, though, they rapidly lose weight and body fat, but not muscle tissue (Forbes et al.,
2001). Leptin injections can produce the same changes in normal animals, too (Fox &
Olster, 2000). These results initially raised hope that leptin might be a “magic bullet”
for treating human obesity, but this is not the case. Although it can help those rare
individuals whose fat cells make no leptin (Farooqi et al., 1999), injections of leptin are
Signals from the Blood
hunger The general state of wanting
to eat.
satiety The condition of no longer
wanting to eat.