Ingestive Behaviors Flashcards
1
Q
What is set point theory?
A
- goal: achieve homeostasis - like a thermostat~ would need detectors to monitor the temperature
- hunger and thirst may operate the same way
2
Q
What does the month do?
A
- physical chewing breaks down food
- saliva moistens food and buffers pH
- food mass is called a bolus
3
Q
What does the esophagus do?
A
- peristalsis: waves that push the food toward the stomach
4
Q
What does the small intestine do?
A
- completes digestion of the food
- absorbs nutrients through the lining
5
Q
What does the large intestine do?
A
- absorbs water from indigestible food material
- sends the rest out of the body as waste
6
Q
What does pepsin do in the stomach?
A
- enzyme that breaks down food
7
Q
What else about the acid in the stomach?
A
- highly acidic: kills microorganisms and also helps to break down food
8
Q
What about bolus and stomach juices?
A
- bolus + stomach juices = chyme
9
Q
Does the stomach help us feel full?
A
- 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
10
Q
Is the stomach the hunger center?
A
- the stomach may release neuropeptides that serve as hunger cues
- BUT - removing the stomach still leads to normal eating behavior
11
Q
What important findings were found?
A
- 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
12
Q
So, what is in the blood?
A
- 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
13
Q
What is 1 problem with the glucostatic theory?
A
- 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
14
Q
What are glucoreceptors?
A
- 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
15
Q
What does leptin do?
A
- 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
16
Q
What about leptin, genetics, and human obesity?
A
- 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
17
Q
What about leptin as an obesity treatment?
A
- 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
18
Q
Short term and long term hunger?
A
- glucose utilization may be monitored for shirt term hunger
- leptin levels and fat stores may be more important for long term hunger
19
Q
What does cholecystokinin (CCK) do?
A
- 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?
20
Q
What does neuropeptide Y (NPY)?
A
- 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
21
Q
What does ghrelin do?
A
- 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
22
Q
Whihc brain structures monitor it?
A
- ventromedial hypothalamus (VMH): lesions lead to overeating, stimulation leads to satiety
- lateral hypothalamus (LH): lesions lead to starvation, stimulation leads to eating
23
Q
What more on the VMH?
A
- 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
24
Q
What more on the LH?
A
- 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
25
Q
What about thirst?
A
- two types of thirst:
- osmometric: detects water movement in and out of cells
- volumetric: detects less of volume in extracellular fluid
26
Q
What brain structures monitor thirst?
A
- lamina terminalis: borders the ventricles in the brain, contains cells outside of the blood brain barrier too ~ able to more easily monitor fluid levels
