Ps219: Homeostasis- Control Of Eating Behaviours

Front 1

Define homeostasis

Back 1

actively keeps an organism's internal state within a critical range

Front 2

What are the internally & externally generated environmental conditions that change constantly?

Back 2

internally generated: nutrients used up, waste products accumulate, growth & reproduction

externally generated: temperature, light VS dark, availability of nutrients.

Front 3

What are the 2 main features of homeostatic systems?

Back 3

1. controlled by negative feedback loops (eg. room temp control)

2. produced oscillating behaviour around a set point - never stops at the set point

Front 4

What are the main 4 nutritional reasons why we need to eat?

Back 4

1. essential amino acid --> building blocks of protein

2. essential fatty acid --> building blocks of fat

3. minerals --> iron, sodium, calcium

4. vitamin --> important for enzymes

Front 5

What 3 "substances" help generate energy?

Back 5

1. carbohydrates

2. fats

3. proteins

Front 6

What are the short VS long term controls of eating behaviours?

Back 6

short term: when to start & end a meal

long term: store energy, release stored energy, anticipate need for energy & nutrients

Front 7

How does short & long-term control of eating behaviours interact?

Back 7

meal size & frequency determines long-term body weight

Front 8

What are the 2 homeostatic & 2 non-homeostatic factors of short-term eating control?

Back 8

1. biochemical signals indicate the state of the energy stores

2. systems/structures detect & interpret signals

1. learning- adapting the system to specific environment

2. mood as a non-adaptive factor

Front 9

Describe the process to create an energy-creating sequence

Back 9

1. eat fats or carbs or proteins

2. digest

3. "turns into" fatty acids or glucose or amino acids

4. further break down occurs

5. acetyl-CoA

6. citric acid cycle OR oxidative phosphorylation

7. ATP (stores energy)

Front 10

How does ATP act as a "rechargeable battery"?

Back 10

stores energy through having phosphate ions, without it, energy is released.

rechargeable via being "charged" with phosphate ions

Front 11

What are the 4 ways available energy can be used for?

Back 11

1. basal metabolism (keeps the cell alive)

2. active behaviour

3. digestion

4. reservation

Front 12

How can basal metabolism be reduced?

Back 12

when the intake of calories is reduced

after fasting, the basal metabolism fills up faster and everything automatically goes to the reserve

Front 13

What does basal metabolism adjust to?

Back 13

caloric intake

Front 14

How can excess energy be stored in the short VS long term?

Back 14

short term: liver & muscles store glucose as glycogen

long term: fat cells store fat

Front 15

How can stored energy become useable energy again?

Back 15

has to be converted/broken down again

Front 16

What do neurons use?

Back 16

glucose

Front 17

What is the role of insulin as a protein hormone?

Back 17

converts glucose into glycogen

Front 18

What is the role of glucagon?

Back 18

converts glycogen back into glucose

Front 19

What do other body cells use (except for red blood cells)?

Back 19

1. fatty acids

2. glucose with insulin

Front 20

Where is insulin produced?

Back 20

pancreas

Front 21

What does released insulin allow the body to do?

Back 21

1. make direct use of some glucose provided by a meal.

2. store some of the glucose (as glycogen) for later use

Front 22

What is the order of the 3 multiple systems/phases that control insulin release?

Back 22

1. cephalic phase (before meal) - signal from the brain

2. digestive phase (during meal) - signal from gut hormone

3. absorptive phase (after meal) - signals from the liver

- evidence from antagonists

Front 23

What is the experimental evidence that blood levels of INSULIN are a crucial signal for eating control?

Why does it have to be rejected?

Back 23

hypothesis: low levels = start of meal VS high levels = end of meal

evidence:

- low blood insulin = animal keeps eating

- inject insulin = animal eats less

BUT...injecting more insulin causes the animal to eat more instead.

Front 24

What is the possible explanations for why animals eat more when injected with insulin despite it theoretically being that they should stop?

Back 24

high insulin levels convert all glucose into glycogen

HENCE

glucose levels are now low, signalling 'hunger'

Front 25

What is the experimental evidence that blood levels of GLUCOSE are a crucial signal for eating control?

Back 25

hypothesis: low levels = start of the meal & high levels = end of the meal

evidence:

- low blood glucose levels = animal keeps eating

- inject glucose = animal eats less

Front 26

What are the problems with the experimental evidence that blood levels of GLUCOSE are a crucial signal for eating control?

Back 26

1. glucose levels do not vary much during the day

2. diabetics: highly increased glucose levels but often feel constant hunger

3. injecting glucose into VMH does not make the animal eat less even though it should

Front 27

What is the experimental evidence that the utilisation of glucose is a crucial signal for eating control? (integrated view)

Back 27

hypothesis: start meal when glucose levels in the liver are low (stored as glycogen) & end meal when the liver gets lots of glucose

evidence:

- liver sends signal to brain via vagus nerve or provides the liver with glucose --> no signal produced.

- reduce eating in hungry animals

- when liver does not signal "low glucose levels" the animal does not act hungry

Front 28

What is the problem with the experimental evidence that the utilisation of glucose is a crucial signal for eating control? (integrated view)

Back 28

reduced eating after cutting the vagus nerve is only temporary

after some time, normal eating behaviours return even though the nerve does not grow back

Front 29

What are the 3 other satiety signals?

Back 29

1. blood levels of free fatty acid

2. blood levels of CKK (a hormone released by intestines in the presence of fat)

3. gut distension

- all show the same problems as previously discussed

Front 30

What are the main 2 conclusions in relation to what signals are involved in eating control?

Back 30

1. no single signal is under all conditions necessary & sufficient for controlling meal size & frequency

2. several signals integrated & utilised in varying combinations

Front 31

What are the 2 centres involved in eating control?

Back 31

VMH - the ventromedial nucleus of the hypothalamus

LH

Front 32

What happens when the VMH is lesioned & stimulated?

Back 32

stimulation - reduced eating

lesion - overeating

- satiety centre

Front 33

What happens when the LH is lesioned & stimulated?

Back 33

stimulation - overeating

lesion - aphagia (no eating)

- hunger centre

Front 34

What is the evidence against the 'dual centre' hypothesis?

Back 34

VMH lesioned rats: defend new body weight just as well as unlesioned rats

- less likely to eat bitter food than normal controls, even if hungry

LH lesioned rats: return back to pathological body weight when force-fed after not eating.

Front 35

What are the main 4 networks involved in regulating eating?

Back 35

1. peripheral structures (liver, intestines)

2. brainstem centres

3. hypothalamic nuclei (LH & VMH)

4. higher brain areas (limbic system)

- system relatively failsafe ~ if one system no longer operates properly then other components make up for it.

Front 36

What is the most important determining factor that signals mealtimes?

Back 36

time of day - learned cue --> hunger

- associations to food can also trigger the desire to eat

Front 37

What role does emotional learning have in eating control?

Back 37

the role of pleasure

- the anticipation of pleasurable food can stimulate hunger

- sensory-specific satiety: monotonous diet reduced appetite.

Front 38

What role does mood have in eating control?

Experimental evidence from Meyer & Wallace (1999)

Back 38

do people eat more when they are feeling 'down'?

- neutral, appetitive or emotional words

- ppts primed with abandonment related emotional words ate more

Front 39

What type of tissue plays an active role in eating control?

Back 39

fat tissue

Front 40

What is the key hormone involved in eating behaviours?

Back 40

leptin

Front 41

What happens if an animal has a defective leptin receptor?

Back 41

becomes obese

Front 42

What is the role of leptin?

Back 42

acts as a satiety centre

- injecting obese rats with leptin results in drastic weight loss

Front 43

What are the steps in creating a model of leptin control on eating behaviours?

Back 43

1. fat cells deplete

2. no leptin is released

3. no leptin arrives at the hypothalamus

4. hypothalamus produces activating signals

5. appetite increases (LH)

6. fat cells fill up

7. fat cells produce & release leptin

8. leptin arrives at the hypothalamus

9. hypothalamus produces inhibiting signals

10. appetite decreases (VMH)

11. fat cells begin to deplete

Front 44

Can the body produce essential or non-essential amino acids?

Back 44

non-essential amino acids

(essential amino-acids come from someones diet)

Front 45

What is the experimental evidence supporting the 'dual centre' hypothesis?

Back 45

1. lesion to the VMH causes overeating

2. lesion to the LH causes aphasia

3. electrical stimulation of the VMH reduces eating

4. electrical stimulation of the LH causes overeating