Stuff to know about HUNGER

(prepared by W. J. Wilson, Fall 2001)

Cannon's Peripheral Theory (early 1900s)

1. Hunger is caused by the walls of an empty stomach rubbing together.
2. Evidence: his graduate student swallowed a balloon that could be inflated in the stomach, in order to measure contractions of the stomach.  Student reported hunger at same time that stomach was contracting
3. Problem:  Correlational! Can't infer causation from correlation.
4. Hunger remains, essentially unchanged, in people and non-human animals whose stomachs have been removed.

 

Dual Center Model (focusing on brain areas)

1. Lesions of ventromedial hypothalamus cause animals to become tremendously obese.
2. Stimulation of this area causes animals to stop eating.
3. Conclusion: this must be the satiety center that tells organism when it is full.
4. Problem: animal eventually does stop eating and maintains a new (much higher than normal) weight.
5. However, notion that VMH is a satiety center persisted.

 

1. Lesions of the lateral hypothalamus cause animals to stop eating, and eventually die unless great effort is made to keep them alive.
2. Stimulation of the LH causes an animal to eat.
3. Conclusion: LH must be feeding (or hunger) center that tells organism when it should start eating.
4. Problem: if nursed back to "health," LH-lesioned animal will eat again, but never normally and never enough to regain the weight that was lost.
5. However, notion that LH is hunger center has persisted.

 

The New View (what these areas are really doing)

1. LH monitors glucose needs.
2. Damage to LH interferes with animal's ability to recognize when glucose levels drop, so it doesn't start eating when this occurs.
3. VMH monitors fat stores by inhibiting the secretion of insulin.
4. Insulin promotes the storage of fat, and prevents the "burning" of fat for energy.
5. Damage to the VMH causes a loss of inhibition of insulin, so animal stores more glucose as fat, and doesn't burn fat.
6. VMH-lesioned rats will get fat even if fed the same amount of food as control rats -- they store more of it as fat.

 

Interesting factoids about Hunger-related stuff:

Work by Schacter:

1. VMH-lesioned rats and obese humans are similar in interesting ways:
2. Both are more "finicky" than controls.  VMH-lesioned rats don't eat as much of a bad tasting food as do control rats.  Obese humans don't drink as much of a bad-tasting milk shake as do control humans.
3. Both are less willing to work for food.  VMH-lesioned rats don't bar-press for food on "lean" schedules, say FR-10, as readily as do the control rats.  Obese humans eat fewer peanuts than do control humans if they have to shell them, but more if they don't have to do this work.
4. These findings support Schacter's conclusion that  both VMH-lesioned rats and obese humans are more sensitive to external cues related to food than to the internal cues provided by their bodies.
5. Obese humans are more likely to eat more when they are misled into thinking it's lunchtime than are control humans - again evidence of the influence of external cues.

 

Diet Pop makes rats fat!

1. Any sweet taste causes an increase in insulin secretion, in preparation for the coming increase in glucose to be stored.
2. Normal Pop provides glucose to store - rats store it away in response to the insulin surge.
3. Diet Pop causes the insulin surge, but does not provide glucose. The insulin surge causes the rats to store away whatever glucose is already circulating, and the LH then causes hunger in response to the drop in glucose.  The rats then eat more than the rats getting Normal Pop, and gain more weight.