The role of neural mechanisms in eating and satiation
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The role of neural mechanisms in eating and satiation. Eating behaviour. Learning objectives. You will be able to: Understand the role of neural mechanisms involved in controlling eating and satiation Evaluate research into the mechanisms of eating and satiation. Q. 7 January 2012.

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Learning objectives
Learning objectives

  • You will be able to:

  • Understand the role of neural mechanisms involved in controlling eating and satiation

  • Evaluate research into the mechanisms of eating and satiation


Q 7 january 2012
Q. 7 January 2012

  • Discuss neural mechanisms involved in the control of eating behaviour.

  • (8 marks + 16 marks)


Mark scheme
Mark scheme

  • Eating behaviour covers all aspects of normal eating behaviour and eating disorders.

  • However candidates are likely to focus on hypothalamic feeding and satiety centres and the dual centre model of feeding regulation.

  • This model also involves the role of hormones such as CCK, leptin and ghrelin. As long as the role of hormones is explicitly linked to neural mechanisms in the brain this approach is fully acceptable. Descriptive terms such as ‘neurotransmitter’ would also be sufficient as a link to neural mechanisms eg in relation to neuropeptide Y and serotonin.

  • Answers that focus, for instance, on eating disorders, should be assessed on the degree to which neural (brain) mechanisms are involved.

  • There are no partial performance criteria on this question. It is hard to imagine an answer considering a single mechanism, but any such answer would be limited and unlikely to move beyond Basic.


Examiner s tip
Examiner’s tip

  • The biology of eating behaviour is very complicated.

  • You need a basic knowledge of the need for control of food intake and body weight, and some of the key processes involved.

  • Focus =

  • The key centres in the hypothalamus need signals to tell them when to start and when to stop feeding.

  • You should be able to outline at least two of these signals.


Hypothalamic feeding and satiety
Hypothalamic feeding and satiety

  • Hetherington and Ranson (1942)

  • Lesions in the hypothalamus of the brain in rats caused the rats to overeat and become obese.


Ventromedial nucleus
Ventromedial nucleus

  • The lesion was in the ventromedial nucleus of the hypothalamus and the rat became known as

  • The VMH rat.


Anand and brobeck 1951
Anand and Brobeck 1951

  • Found that a lesion in the lateral hypothalamus (LH) led to a loss of feeding in rats known as

  • Aphagia

  • They assumed the function of the LH was to stimulate feeding in hungry rats.


The satiety centre
The satiety centre

  • The lesion destroyed a vital centre for the control of feeding behaviour.

  • Its destruction led to an increase in feeding and body weight.

  • Hetherington and Ranson assumed this was a ‘satiety centre’.

  • They assumed it was normally activated when the animal was full and its function was to inhibit feeding.


Dual centre model of feeding
Dual-centre model of feeding

  • Later studies confirmed previous findings.


Processes involved
Processes involved

  • The dual model is confirmed by much research but the pathways are very complex.



Eating schedules
Eating schedules

  • In Western countries we usually eat to a schedule. The digestive system starts preparing itself by releasing saliva and enzymes just before a meal time (Pinel, 2007). This represents a learned response, anticipating the presence of food.



Prepare the digestive system
Prepare the digestive system

  • Even when we’re not really hungry, we can be tempted by some things.


When we are hungry
When we are hungry

  • The empty stomach sends signals to the brain to start eating.

  • An important role is played by a hormone –

  • Grehlin


Ghrelin
Ghrelin

  • Ghrelin is a hormone that signals the hypothalamus to stimulate feeding.

  • The amount released is directly proportional to the emptiness of the stomach.

  • As the time from the last meal increases so ghrelin secretion is increased.


Research evidence
Research evidence

  • Injections of ghrelin increase food intake and body weight in animals and humans (Cummings, 2006).

  • Gastric bands used to treat obesity reduce ghrelin secretion from the stomach.


Ghrelin and the brain
Ghrelin and the brain

  • Cummings (2006) found that ghrelin acts directly on the brain mechanisms of feeding behaviour, including the hypothalamus.


Cummings et al 2004
Cummings et al. (2004)

  • Investigated changes in blood ghrelin levels over time between meals.

  • 6 participants ate lunch.

  • Their ghrelin levels were measured from blood samples taken every 5 minutes until they requested their evening meal.



Findings
Findings

  • Ghrelin levels fell immediately after eating lunch

  • The lowest level was after about 70 minutes.

  • Then they slowly began to rise

  • Peaking as participants requested their evening meal.


Findings continued
Findings continued

  • Ghrelin levels positively correlated with the degree of hunger reported in 5 out of the 6 participants.

  • Conclusion – ghrelin levels directly reflect stomach emptiness and are closely related to feelings of hunger.


Conclusion
Conclusion

  • This supports a role for ghrelin in signalling appetite in humans.


Signals stopping the intake of food
Signals stopping the intake of food

  • Leptin is a hormone released from fatty (adipose) tissue.

  • It acts as an indicator of body weight to hypothalamic mechanisms controlling long-term food intake.


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