Eating Behaviour

Question 1

What is a behaviour?

What is motivation?

Answer 1

the response of an organism to a stimulus
-can be: 1)conscious 2)unconscious
-higher level voluntary or conscious behaviours require motivation
motivation = driving force behind a behaviour and can be simple or complex

Question 2

The ‘WC’ model?
(using water cistern as example)
limitations?

Answer 2

the water cistern fills up (increased motivation) until limit is reached
flushing releases behaviour and motivation is low
gradually motivation builds back up again until there’s another release
limitation = this model has many flaws: human behaviour is much more sophisticated
-probability and direction of a behaviour will vary with driving force
-motivation may be required for a behaviour but it doens’t guarantee it! (cultural, personal, social influences)
-balance conflicting motivations

Question 3

More basic survival behaviours can be explained to some extent

• controlled by?
• developed where in brain?
• central part of homeostatic mechanisms control what?
• what is ‘energy balance’?
• building up macromolecules is called =
• breaking down macromolecules is called=

Answer 3

controlled by hypothalamus
develops from the diencephalon of the forebrain
central part of the homeostatic system controls eating and sexual behaviour
energy balance required= balance between bodies intake and output of energy
building up= anabolism
breaking down = catabolism

Question 4

Energy in the body
requirements change because of?
Anabolism > catabolism =
Anabolism < catabolism =

Answer 4

requirments for energy in the body = continuous
(few mins without glucose can kill neurons)
Requirements can change depending on:
-time of day/month/year/ life
-level of activity
-state of health
A>C = obesity
A

Question 5

History found:
what caused anorexia?
contrasting research?

Answer 5

lesions on both sides of a rats lateral hypothalamus caused anorexia
contrast= found bilateral lesions of the ventromedial hypothalamus caused overeating and obesity
Historically, hypothalamus was called the ‘hunger centre’ and the ventromedial hypothalamus the ‘satiety centre’

Question 6

Long term regulation of feeding?

• Kennedy (1953)
• Coleman?

Answer 6

K proposed brain monitors fat levels and acts to maintain them (lipostatic hypothesis)

• signal from fat to brain was hypothesised to tell brain about fat levels
• Coleman proposed a soluble factor in obese mice fooled the brain into thinking that fat levels were normal, so the mouse continued to eat

Question 7

Friedman (1994)
Leptin?
Starvation
Obesity

Answer 7

F- isolated protein responsible! LEPTIN!
Leptin = released by fat cells to decrease eating behaviour and increase energy expenditure
Starvation –>leptin deficiency stimulates eating behaviour, decreases energy expenditure and reduces reproductive competence
- HIGH levels of leptin act on receptors on neurons in ARCUATE NUCLEUS of the hypothalamus
-These neurons release NETS: alpha-MSH and CART
-LOW levels of leptin switch off alpha-MSH and CART NET release but stimulate other neurons in arcuate nucleus releasing NPY amd AgRP

Question 8

How does high leptin level work?

How does it cause anorexia?

Answer 8

• stimulation of the paraventricular nucleus acts to release TSH and ACTH from the anterior pituitary gland
• TSH and ACTH act on the thyroid and adrenal glands to increase basal metabolic rate
• these inputs stimulate a co-ordinated response to high leptin (high fat) levels
• Stimulation of the brainstem and upper spinal cord increases SYMPATHETIC activity causing raised body temp (and increase BMR)
• Feeding behaviour is inhibited by somatic motor activity through stimulation of cells in the lateral hypothalamus
• injection of alpha-MSH and CART mimic effect of raised leptin levels and can be called anorectic peptides(appetite suppressors)

Question 9

What happens when there is a low level of leptin?

Sympathetic or para?

Answer 9

• Low levels of leptin inhibit TSH and ACTH secretion
• activate PARASYMPATHETIC nervous system
• stimulate feeding behaviour
• are called orexigenic peptides
• Gherelin = released into bloodstream from an empty stomach and stimulates NPY and AgRP

Question 10

Short-term regulation

Answer 10

Short term factor also influence daily food intake (eg cultural norms - eating times)
-motivations to continue eating a meal depends on what and how much we’ve already eaten
SO, long term regulation is modified by short term signals generated when we eat
=satiety signals

Question 11

satiety signals=?

Answer 11

produced when we eat and during initial digestion (the prandial period)
-they terminate eating and inhibit future eating
Decline in satiety signal= orexigenic signals dominate and stimulate feeding
-satiety terminates feeding, such as distension in stomach, insulina nd cholecystokinin

Question 12

Other aspects of feeding?

Answer 12

enjoy eating = hedonistic motivation
mood and food - some foods produce changes via serotonin
so, - post-absorption of food elevates serotonin levels
-typical to see carb-rich feeding during stress
Some drugs that elevate serotonin inhibit appetite
Anorexia and Bulimia can be linked to serotonin levels
Proxac and other increasing serotonin drugs can relieve bulimia and depression