Control of Food Intake
Key Points:
A description of the differences between hunger, appetite and satiety
A discussion of the role of afferent nerves (particularly vagal) from the stomach and
small intestine in the regulation of food intake and the genesis of the sensation of
‘fullness’
A review of how an impaired ability of the stomach to accommodate and a delay in the
rate of gastric emptying can give rise to ‘early satiety’
An overview of the role of endocrine (hormones) and post-absorptive signals in the
short and long term regulation of food intake. The lecture will focus on a few examples
(e.g. cholecytstokinin, obestatin, leptin, ghrelin) as this is a very complex area
Definitions
Satiety = State of being full after eating food
Appetite = Describes the desire to satisfy the body’s needs of food
Hunger = Discomfort caused by lack of food and the desire to eat – a strong craving for
food
Aphagia = The inability or refusal to swallow
Hyperphagia/polyphagia = An abnormal desire for food (extreme unsatisfied drive to
eat)
Control of Food Intake
The main control of food intake is the hypothalamic control
- Young people can maintain a constant body weight, but the ability to do this
decreases with age (middle aged spread)
Reasons for differences in BMI
-> Genes
-> How much we eat and its consumption
Central Control of Food Intake: Where is the Switch?
We can associate two aspects of this ‘switch’ to the hypothalamus, the satiety centre
and the feeding centre.
The satiety centre is in the ventromedial wall of paraventricular nucleus (PVN) (in
hypothalamus) and stimulation of this causes aphagia.
Lesions of the ventromedial wall of paraventricular nucleus lead to hyperphagia
(increased appetite or excessive hunger)
The feeding centre is in the lateral hypothalamus, stimulation of it will increase
feeding. While lesions of this region cause aphagia.
The brain has a glucostat, it can measure the amount of glucose that is reaching it
because it relies on it so heavily.
, There are also various molecules that are important in modulating how much we eat,
these include: opioids, somatostatin, growth hormone releasing hormone = Increase
appetite.
However we also need to remember that there are afferent signals reaching the brain,
there are signals coming from the periphery (around us) and CNS.
Higher functions also modulate responses to both CNS (what is inside us) and
peripheral cues (what is around us) which lead to inhibition or stimulation of intake
Factors that affect if food is sought or not and the type we ingest include:
-Food preferences
-Emotions
-Environment
-Life style
-Circadian rhythm
Anorexigenic factors are molecules that suppress appetite such as: 5-HT (5-HT 2c and
5-HT1A), dopamine and GABA. If you inject these into the hypothalamus you will see a
decrease in appetite.
Cortical and limbic centres of food intake are important in habit and conditioning
(seeking food, what food is around us, in our body)
There is also diurnal variation in food intake ->
Carbohydrates are metabolised during the day whereas fats are metabolised at night.
The hypothalamus responds (senses) to the switch between carbohydrate and fat
metabolism.
Control of Food Intake: What Signals Our Appetite?
As mentioned earlier the brain has a glucostat, the concentration of glucose in the
blood will stimulate glucoreceptors in the hypothalamus. This means we have to take
glucose up.
Decreased blood glucose will up-regulate hunger while increased blood glucose will
up-regulate satiety.
->Diabetics feel hungry despite increased glucose. This is because blood glucose is not
entering the cells, so the body isn’t sensing this.
-> Cold environments simulate feeding while hot environments inhibit appetite. This is
useful as allows to put fat on when cold.
Afferent Input
-> Distension of a full stomach inhibits appetite, contraction of an empty one
stimulates appetite both via afferents
-> Denervation of intestine and stomach seems to have no effect on food intake, tells
us there are other things going on
-> Deposition of fat may control appetite, as fat tissue has ability to release leptin
(more fat = more leptin)
Key Points:
A description of the differences between hunger, appetite and satiety
A discussion of the role of afferent nerves (particularly vagal) from the stomach and
small intestine in the regulation of food intake and the genesis of the sensation of
‘fullness’
A review of how an impaired ability of the stomach to accommodate and a delay in the
rate of gastric emptying can give rise to ‘early satiety’
An overview of the role of endocrine (hormones) and post-absorptive signals in the
short and long term regulation of food intake. The lecture will focus on a few examples
(e.g. cholecytstokinin, obestatin, leptin, ghrelin) as this is a very complex area
Definitions
Satiety = State of being full after eating food
Appetite = Describes the desire to satisfy the body’s needs of food
Hunger = Discomfort caused by lack of food and the desire to eat – a strong craving for
food
Aphagia = The inability or refusal to swallow
Hyperphagia/polyphagia = An abnormal desire for food (extreme unsatisfied drive to
eat)
Control of Food Intake
The main control of food intake is the hypothalamic control
- Young people can maintain a constant body weight, but the ability to do this
decreases with age (middle aged spread)
Reasons for differences in BMI
-> Genes
-> How much we eat and its consumption
Central Control of Food Intake: Where is the Switch?
We can associate two aspects of this ‘switch’ to the hypothalamus, the satiety centre
and the feeding centre.
The satiety centre is in the ventromedial wall of paraventricular nucleus (PVN) (in
hypothalamus) and stimulation of this causes aphagia.
Lesions of the ventromedial wall of paraventricular nucleus lead to hyperphagia
(increased appetite or excessive hunger)
The feeding centre is in the lateral hypothalamus, stimulation of it will increase
feeding. While lesions of this region cause aphagia.
The brain has a glucostat, it can measure the amount of glucose that is reaching it
because it relies on it so heavily.
, There are also various molecules that are important in modulating how much we eat,
these include: opioids, somatostatin, growth hormone releasing hormone = Increase
appetite.
However we also need to remember that there are afferent signals reaching the brain,
there are signals coming from the periphery (around us) and CNS.
Higher functions also modulate responses to both CNS (what is inside us) and
peripheral cues (what is around us) which lead to inhibition or stimulation of intake
Factors that affect if food is sought or not and the type we ingest include:
-Food preferences
-Emotions
-Environment
-Life style
-Circadian rhythm
Anorexigenic factors are molecules that suppress appetite such as: 5-HT (5-HT 2c and
5-HT1A), dopamine and GABA. If you inject these into the hypothalamus you will see a
decrease in appetite.
Cortical and limbic centres of food intake are important in habit and conditioning
(seeking food, what food is around us, in our body)
There is also diurnal variation in food intake ->
Carbohydrates are metabolised during the day whereas fats are metabolised at night.
The hypothalamus responds (senses) to the switch between carbohydrate and fat
metabolism.
Control of Food Intake: What Signals Our Appetite?
As mentioned earlier the brain has a glucostat, the concentration of glucose in the
blood will stimulate glucoreceptors in the hypothalamus. This means we have to take
glucose up.
Decreased blood glucose will up-regulate hunger while increased blood glucose will
up-regulate satiety.
->Diabetics feel hungry despite increased glucose. This is because blood glucose is not
entering the cells, so the body isn’t sensing this.
-> Cold environments simulate feeding while hot environments inhibit appetite. This is
useful as allows to put fat on when cold.
Afferent Input
-> Distension of a full stomach inhibits appetite, contraction of an empty one
stimulates appetite both via afferents
-> Denervation of intestine and stomach seems to have no effect on food intake, tells
us there are other things going on
-> Deposition of fat may control appetite, as fat tissue has ability to release leptin
(more fat = more leptin)
