Ingestive Behaviors

Question 1

What is set point theory?

Answer 1

• goal: achieve homeostasis - like a thermostat~ would need detectors to monitor the temperature
• hunger and thirst may operate the same way

Question 2

What does the month do?

Answer 2

• physical chewing breaks down food
• saliva moistens food and buffers pH
• food mass is called a bolus

Question 3

What does the esophagus do?

Answer 3

• peristalsis: waves that push the food toward the stomach

Question 4

What does the small intestine do?

Answer 4

• completes digestion of the food
• absorbs nutrients through the lining

Question 5

What does the large intestine do?

Answer 5

• absorbs water from indigestible food material
• sends the rest out of the body as waste

Question 6

What does pepsin do in the stomach?

Answer 6

• enzyme that breaks down food

Question 7

What else about the acid in the stomach?

Answer 7

• highly acidic: kills microorganisms and also helps to break down food

Question 8

What about bolus and stomach juices?

Answer 8

• bolus + stomach juices = chyme

Question 9

Does the stomach help us feel full?

Answer 9

• hunger pangs are accompanied by stomach contractions
• a stretched stomach leads to changes in the firing rate of hypothalamic cells
• removing food from the stomach leads to eating
• increasing food in the stomach leads to reduction in eating

Question 10

Is the stomach the hunger center?

Answer 10

• the stomach may release neuropeptides that serve as hunger cues
• BUT - removing the stomach still leads to normal eating behavior

Question 11

What important findings were found?

Answer 11

• when blood transfusions were made from well fed rats to food-deprived rats, they stopped eating
• there must be something in the blood that makes them hungry/full

Question 12

So, what is in the blood?

Answer 12

• glucostatic theory: states that glucose levels of the most important hunger cue
• injecting glucose into hungry animals suppresses eating ~ injecting insulin (lowers glucose levels) INCREASES eating
• glucose levels drop 10 minutes before a meal
• injecting glucose at that time can PREVENT the meal

Question 13

What is 1 problem with the glucostatic theory?

Answer 13

• diabetes patients: low/no insulin levels, leads to high glucose levels, often quite hungry
• maybe it is not about the gross amount or concentration of glucose in the blood but about how much glucose is utilized for energy processes- diabetics would have high glucose levels, but low utilization

Question 14

What are glucoreceptors?

Answer 14

• found in the brain and liver
• thioglucose studies: mimics glucose but is toxic to the receptors
  ~ damages the ventromedial hypothalamus ~ injecting glucose in the ventromedial hypothalamus does not suppress hunger
  ~ sugars that are processed in the liver, and are unable to cross the blood-brain barrier, like fructose, still lead to satiety ; but severing the connections between the liver an the brain do not change eating behaviors

Question 15

What does leptin do?

Answer 15

• leptin deficient (genetically deficient) mice were discovered: were obese, could weigh up to 3x normal, leptin injections led to 30% loss in body weight
• leptin comes from body fat: more fat = more leptin
• may work in the hypothalamus: inhibits neuropeptide Y , NPY triggers eating behaviors

Question 16

What about leptin, genetics, and human obesity?

Answer 16

• genetic deficiencies of leptin in humans is rare
• 8 year old girl w/57% body fat and weighed nearly 190 pounds
• 2 year old male w/54% body fat and weighed nearly 64 pounds

Question 17

What about leptin as an obesity treatment?

Answer 17

• obese people typically have more leptin
• maybe they have a reduced sensitivity
• injecting leptin as a dieting agent for normal obese people has not led to good results

Question 18

Short term and long term hunger?

Answer 18

• glucose utilization may be monitored for shirt term hunger
• leptin levels and fat stores may be more important for long term hunger

Question 19

What does cholecystokinin (CCK) do?

Answer 19

• released in the small intestine at the presence of fat and protein
• injecting CCK stops eating behaviors
• CCK blocking drugs lead to eating
• CCK receptors are in the ventromedial hypothalamus
• PROBLEM: CCK leads to nausea- maybe thats why it reduces eating?

Question 20

What does neuropeptide Y (NPY)?

Answer 20

• injection leads to voracious eating - focuses on carbohydrates
• CCK suppresses NPY ~ CCK suppresses the appetite
• found in the hypothalamus
• PROBLEM: NPY is the most abundant neuropeptide in the brain ~ linked to memory, body temperature, blood pressure, sexual function
• found all over the brain as well

Question 21

What does ghrelin do?

Answer 21

• levels increase when fasting
• drop after a meal
• targets receptors in the arcuate nucleus of the hypothalamus
• tied more to glucose levels than fat/protein levels
• breaks down into obestatin which decreases food intake

Question 22

Whihc brain structures monitor it?

Answer 22

• ventromedial hypothalamus (VMH): lesions lead to overeating, stimulation leads to satiety
• lateral hypothalamus (LH): lesions lead to starvation, stimulation leads to eating

Question 23

What more on the VMH?

Answer 23

• when lesioned: rats ate continually at first, doubled body weight in weeks, only temporary
• may control insulin levels: increases in insulin levels reported after lesions, increased insulin increases eating, damage may change the amount of insulin being released

Question 24

What more on the LH?

Answer 24

• lesioned rats starved themselves: can be overcome by force feeding, eventually force-fed rats eat on their own
• may be linked to REWARD systems
• may be linked to ATTENTION : damaging the LH can lead to sensory neglect , if pinched (stimulated), rats with LH damage will eat

Question 25

What about thirst?

Answer 25

• two types of thirst:
• osmometric: detects water movement in and out of cells
• volumetric: detects less of volume in extracellular fluid

Question 26

What brain structures monitor thirst?

Answer 26

• lamina terminalis: borders the ventricles in the brain, contains cells outside of the blood brain barrier too ~ able to more easily monitor fluid levels