• Animals vary in their strategies of eating, but
humans tend to eat more than they need at
the given moment.
• A combination of learned and unlearned
factors contribute to hunger.
• The digestive system
• Saliva → carbs
– Hydrochloric acid → proteins
• Small intestine
• Large intestine
• The brain regulates eating through messages
from the mouth, stomach, intestines, fat cells
• The main signal to stop eating is the
distention of the stomach.
– The vagus nerve
– The splanchnic nerves
• Cholecystokinin (CCK)
• Glucose, insulin, and glucagon levels also
influence feelings of hunger (see figures 10-
14, 10-15, 10-6).
Fig. 10-14, p. 311
Fig. 10-15, p. 311
Fig. 10-16, p. 311
• Long-term hunger regulation is accomplished
via the monitoring of fat supplies by the body.
• Information from all parts of the body
regarding hunger impinge into two kinds of
cells in the arcuate nucleus.
• Output from the arcuate nucleus goes to the
paraventricular nucleus of the hypothalamus.
• Input from the hunger-sensitive neurons of
the arcuate nucleus is inhibitory to both the
paraventricular nucleus and the satiety-
sensitive cells of the arcuate nucleus itself.
• Output from the paraventricular nucleus acts
on the lateral hypothalamus.
– The lateral hypothalamus controls insulin
secretion and alters taste responsiveness.
• Animals with damage to this area refuse food
and water and may starve to death unless
Fig. 10-20, p. 315
• The lateral hypothalamus contributes to
Fig. 10-22, p. 316
• Ventromedial hypothalamus → satiety
• People with a mutated gene for the receptors
melanocortin overeat and become obese.
– Melanocortin is a neuropeptide responsible
• Prader-Willis syndrome
• Anorexia nervosa
• Bulimia nervosa
• Overeating and Binge-eating Disorder