Neural and Hormonal Mechanisms Involved in Controlling Eating Behaviour Flashcards
The main area in the brain involved in the regulation of appetite is the:
hypothalamus
The hypothalamus is mainly involved in maintaining:
homeostasis
Homeostasis:
The balancing of hormones to maintain a steady internal environment. Part of the homeostatic mechanism is detecting whether the body has enough nutrients (glucose) and correcting the situation if this is not the case.
Dual centre model
Within the hypothalamus are two significant eating control centres: the lateral hypothalamus and the ventromedial hypothalamus. These two parts work together to control food consumption and weight
Role of the Lateral hypothalamus (hunger centre)
- The LH is associated with hunger. It acts as the ‘on switch’ for eating
- The LH contains cells which detect levels of glucose by communicating with the liver. Liver communicates when there are low levels of glucose.
- When there is a decline in blood glucose levels, this is communicated to the lateral hypothalamus, which leads to the LH stimulating release of neuropeptide Y which is an appetite stimulant.
- This will lead to feelings of hunger and causes us to search for and to eat food which leads to glucose levels rising again.
Role of the Ventromedial hypothalamus (satiety centre)
- Liver cells communicate the rise in glucose level to the ventromedial hypothalamus (known as the satiety centre).
- VHM triggers feelings of satiation (fullness)
- These feelings stop further eating + inhibit eating behavior
- Damage to the VMH leads to inability to stop eating
Hormonal mechanisms involved in eating behaviour:
- leptin
- ghrelin
Leptin:
- Leptin is produced by fat cells and is released into the bloodstream
- The amount of leptin released into your bloodstream is directly proportional to the fat content in your body
- Short term flunctuations in leptin provide the VMH information about your calorie intake
- As we eat, the amount of fat in our body increases, thus leptin release also increases which acts as an appetite suppressant as it leads to the VMH triggering satiety
- It does this by binding to receptors in the VMH which counteracts the appetite stimulant effect of NPY.
- This leads to a reduction in hunger, thus leading to satiety.
Ghrelin:
- Ghrelin is a hormone secreted by the stomach which travels to the hypothalamus before eating and stimulates it to increase appetite. If a person is undereating, their ghrelin levels increase.
- Ghrelin is detected by the arcuate nucleus in the hypothalamus, which signals to the lateral hypothalamus to release NPY, triggering hunger.
- It is a hormonal marker of how long since we have last eaten bc the amount produced is closely related to how empty your stomach is (emptier the stomach, higher the levels of ghrelin). The amount of ghrelin in the bloodstream doubles just before a meal and decreases very quickly after a meal.
Evals:
+ A strength of the Dual Centre Model: supporting evidence.
- A weakness of research into the neural/hormonal mechanisms behind eating behaviour is that there are issues with animal extrapolation.
- A strength of hormonal explanation in EB: support for the role of leptin.
- A strength of hormonal explanation in EB: support for the role of ghrelin.
+ A strength of the Dual Centre Model: supporting evidence.
Anand and Brobeck: found that damaging the lateral hypothalamus in rats led to a loss of interest in food, decreased eating and weight loss.
Hetherington and Ranson: showed damage to the ventromedial hypothalamus led to the animals overeating until they were grossly obese.
SB: validates the supposed roles of each part of the DCM/ The rats losing weight due to damage to lateral hypothalamus proves they did not eat due to a lack of feeling of hunger and that the lateral hypothalamus is responsible for hunger.
Also proves the role of VMH is regarding satiety as when this function is not executed, the rats overate a lot and gain weight.
Increases validity of DCM.
Anand and Brobeck:
found that damaging the lateral hypothalamus in rats led to a loss of interest in food, decreased eating and weight loss.
Hetherington and Ranson:
showed damage to the ventromedial hypothalamus led to the animals overeating until they were grossly obese.
A weakness of research into the neural/hormonal mechanisms behind eating behaviour is that there are issues with animal extrapolation.
Research - mainly done on rats/mice - humans barely suffer damage to hypothalamus.
However, this is an issue bc altho there are broad similarities between humans and brains of other animals, we can’t assume findings always apply to the human brain and endocrine system.
This is because the way humans regulate feeding beh is much more complex. There are differences in how neural / hormonal activity affects eating behaviour between humans compared to animals.
Also, human feeding mechanisms are more complex as humans are affected by influences like conscious choice, health concerns. Such factors do not affect rats, so we cannot apply results from rats to humans to understand eating behaviours.
A strength of hormonal explanation in EB: support for the role of leptin.
Research has shown that some mice receive two copies of the gene for obesity. These ob/ob mice have a tendency to overear especially foods high in sugar or fat.
Zhang et al: discovered that ob/ob mice have defective genes which make them deficient in the hormone leptin. Also, injecting ob/ob mice with leptin causes them to lose weight dramatically.
SB: proves role of leptin - mice overeat as they dont feel satiety.
When injected w/ leptin - lose weight as eating in a regulated way returns - feeling satiety
increase validity of understanding of the role of leptin.
