Motivation and Emotion 369leptin
a hormone that, when released into
the bloodstream, signals the hypothal-
amus that the body has had enough
food and reduces the appetite while
increasing the feeling of being full.Figure 9.4 Obese
Laboratory Rat
The rat on the left has reached
a high level of obesity because
its ventromedial hypothalamus
has been deliberately damaged
in the laboratory. The result is a
rat that no longer receives signals
of being satiated, and so the rat
continues to eat and eat and eat.weight set point
the particular level of weight that the
body tries to maintain.basal metabolic rate (BMR)
the rate at which the body burns
energy when the organism is resting.is such a large amount of glucose released by these foods at one time. High blood
sugar leads to more insulin released, which leads to a low blood sugar level, increased
appetite, and the tendency to overeat. That is the basic principle behind many of the
diets that promote low carbohydrate intake. The proponents of these diets argue that
if people control the carbohydrates, they can control the insulin reaction and prevent
hunger cravings later on.
In recent years, a hormone called leptin has been identified as one of the factors
that seems to control appetite. When released into the bloodstream, leptin signals the
hypothalamus that the body has had enough food, reducing appetite and increasing the
feeling of being full, or satiated. Genetic abnormalities in the receptors for leptin as well
as leptin resistance may play an important role in obesity (Dubern & Clement, 2012; Pan
et al., 2014).
THE ROLE OF THE HYPOTHALAMUS The stomach and the pancreas are only two of
the body parts involved in hunger. In Chapter Two, the role of the hypothalamus in
controlling many kinds of motivational stimuli, including hunger, was seen as a result
of its influence on the pituitary. But the hypothalamus itself has different areas, con-
trolled by the levels of glucose and insulin in the body, which appear to control eating
behavior.
The ventromedial hypothalamus (VMH) may be involved in stopping the eating
response when glucose levels go up (Neary et al., 2004). In one study, rats whose VMH
areas (located toward the bottom and center of the hypothalamus) were damaged would
no longer stop eating—they ate and ate until they were quite overweight (Hetherington &
Ranson, 1940). (See Figure 9. 4 for a picture of a rat with this kind of damage.) However,
they did not eat everything in sight. They actually got rather picky, only overeating on
food that appealed to them (Ferguson & Keesey, 1975; Parkinson & Weingarten, 1990). In
fact, if all the food available to them was unappealing, they did not become obese and in
some cases even lost weight.
Another part of the hypothalamus, located on the side and called the lateral
hypothalamus (LH), seems to influence the onset of eating when insulin levels go up
(Neary et al., 2004). Damage to this area caused rats to stop eating to the point of star-
vation. They would eat only if force-fed and still lost weight under those conditions
(Anand & Brobeck, 1951; Hoebel & Teitelbaum, 1966). Both of these areas of the hypothal-
amus are involved in the production of orexin-A, a neuropeptide (a small, protein-like
molecule that neurons use to communicate) involved in appetite control (Li et al., 2014;
Messina et al., 2014).
WEIGHT SET POINT AND BASAL METABOLIC RATE Obviously, the role of the hypothal-
amus in eating behavior is complex. Some researchers (Leibel et al., 1995; Nisbett, 1972)
believe that the hypothalamus affects the particular level of weight that the body tries
to maintain, called the weight set point. Injury to the hypothalamus does raise or lower
the weight set point rather dramatically, causing either drastic weight loss or weight
gain.
Metabolism, the speed at which the body burns available energy, and exercise
also play a part in the weight set point. Some people are no doubt genetically wired
to have faster metabolisms, and those people can eat large amounts of food without
gaining weight. Others have slower metabolisms and may eat a normal or even less-
than-normal amount of food and still gain weight or have difficulty losing it (Bouch-
ard et al., 1990; Higginson et al., 2016). (Some people swear they can gain weight just
by looking at a piece of cake!) Regular, moderate exercise can help offset the slowing
of metabolism and the increase in the weight set point that comes with it (Tremblay
et al., 1999).
The rate at which the body burns energy when a person is resting is called the basal
metabolic rate (BMR) and is directly tied to the set point. If a person’s BMR decreases (as