Control of Food Intake Flashcards
What are the main substances that control food intake?
When food intakes start there are neural mechanisms that allows the stomach to accommodate it , VIP and NO
When you start emptying the stomach contractions occur, then hunger sets in and one of the factors that’s quite important in that is ghrelin
PYY can lead to a feeling of satiety
How do we accommodate food in the gastric reservoir?
Mechanical stimuli in the pharynx so you take in an amount of food
We have a phenomena called receptive relaxation of the fundus
There is a nervous supply that innervates the vagal centre and there you have inhibitory fibres called NANC (non-adrenergic non-cholinergic) inhibition
The reason for this is because the final mediator is not acetylcholine or adrenaline but acetylcholine is released pre-synaptically
Adaptive relaxation is the stomach adapting to the presence of food in it
The third mechanism that leads to the accommodation is feedback relaxation
The stomach has got its own ‘little brain’ called the enteric nervous system
The enteric nervous system is able to detect what food components we have eaten
Now when you have taken up food containing lipids/fats something called cholecystokinin (CCK) gets released
CCK gives a sense of fullness through stimulating the vagal centre
What is a vagotomy and what does it do?
Vagotomy impairs accommodation and emptying: a cause for early satiety in some patients
1. Vagotomy reduces accommodation and gastric compliance
This is because the fundus is not able to expand and accommodation is inhibited
But also when you have no motor activity, not able to carry out gastric emptying, so you feel bloated for longer, nausea sets in and easy filling
2. In relative terms, denervation of intestines and stomach may have no effect on food intake- signals from pancreas, adipocytes, GIT and CNS
What are the definitions of hunger, appetite and satiety?
Hunger- discomfort caused by lack of food and the desire to eat- a strong physiological craving/drive for food/ sensation of emptiness in stomach
Appetite- physiological desire/drive to satisfy the body’s needs of food; a hunger-stimulated response
Satiety- state of being full after eating food (joyous moments- no longer need to continue)
Aphagia- the inability or refusal to swallow
Hyperphagia/polyphagia- an abnormal desire for food (extreme unsatisfied drive to eat)
What is hypothalamic control of food intake?
“The young can maintain constant body weight”, but their ability to do so decreases with age (-> middle age spread?)
Reasons for differences in BMI:
Genes (70%)
How much we eat and its composition
There is a balance of stimulating and inhibiting forces in the hypothalamus regulates feeding
Diurnal variation in food metabolism:
Carbohydrates metabolised during the day
Fats metabolised at night
Hypothalamus responds to the switch between carbohydrate and fat metabolism
How does the hypothalamus control hunger and thirst?
Hypothalamus- control centre for appetite and food intake
Controls hunger (and thirst)
How does the hypothalamus do that?
The base of the hypothalamus has several nuclei that regulate energy homeostasis
Controls the appetite; size of helping, and out ingestive behaviour
The somatosensory cortex is quite important for taste perception and we can form preferences
Nucleus accumbens controls ingestion and swallowing
Prefrontal cortex is hugely important for food-seeking behaviour
Nucleus of the tractus solitarius is quite important for swallowing behaviour
Where is the satiety centre within the hypothalamus and what does it do?
The satiety centre within the hypothalamus [specifically the ventromedial (wall of paraventricular)nuclei]
Stimulation of ventromedial -> aphagia (swallowing difficulty)
Lesions of ventromedial nuclei -> hyperphagia (increased appetite or excessive hunger; weight gain)
Feeding/hunger/thirst centre- the lateral hypothalamus
Simulation of lateral hypothalamus →↑ feeding
Lesion of this region → aphagia
Substances:
Opioids (growth hormone releasing hormone) →↑ appetite
Naltrexone (opioid antagonist) reduces the positive ‘hedonic valence’ of food
What are five hypothalamic nuclei in control of?
Feeding behaviour/food intake is modulated by the following hypothalamic sites:
1. Lateral hypothalamus (LH)- hunger/thirst centre
2. Ventromedial nucleus (VMN)- satiety centre
What to remember about ventromedial nucleus and lateral hypothalamus
We normally have the ability to restrain feeding if required but; lesion of VMN →↑ appetite, with weight gain that tends to persist
3. Dorsomedial nucleus (DMN)- modulates energy intake (hunger centre)
- release of NPY into DMN →↑ feeding
4. Paraventricular nucleus (PVN)- modulates feeding behaviour
Paraventricular nucleus and perifornical hypothalamus are the centres that control feeding behaviours through:
NPY, opioids, and GABA →↑ feeding while leptin →↓ food intake
5. Arcuate nucleus
Neurons produce orexigenic signals- factors that increase feeding (NPY, the opioids, dynorphin, b-endorphin, POMC, galanin, amino acids, glutamate and GABA) →↑ feeding
Effects of GABA on food intake- GABA has mixed effects on food intake depending on where it acts/is injected
What are the sixth and seventh hypothalamic nuclei in control of?
- Suprachiasmatic nucleus
Human body clock is located in the suprachiasmatic nuclei so controls human body clock
Perception of the light-dark cycle (circadian rhythms)- appetite or the sensation of hunger -> mood/drive to eat- Medial amygdaloid nucleus
A role for medial amygdaloid nucleus in feeding behaviour has been proposed:
It is a sub-region of the amygdaloid complex
Participates in the regulation of food intake
Ligands: 5-HT (via 5-HT2C and 5-HT1A)- regulates appetite and food intake
How?
A is the appetite stimulating pathway while B is the appetite suppressing pathway
So we have our 5-HT neuron which releases 5-HT and that can bind to its receptor and allow POMC to be metabolised
Once metabolised it is converted to alphaMSH
Once alphaMSH is released it can bind to a receptor called MC4R, so when occupied food intake is supressed
So when you feel hungry it is because NPY and AgRP is being released to induce appetite through the appetite stimulating pathway
Meta-chlorophenylpiperazine (mCPP) is a 5-HT2C agonist allows the POMC to be broken down and release alphaMSH to bind to the MC4R causing a decrease in appetite
- Medial amygdaloid nucleus
What are the anorexigenic factors?
5-HT (5-HT2C and 5-HT1A), dopamine, GABA →↓ appetite
These are referred to as anorexigenic factors
What is the effects of zimelidine?
Effects of zimelidine on medial amygdaloid (Medial amygdaloid nucleus)= MeA mediates food intake
Zimelidine- inhibits the reuptake of 5-HT from synaptic cleft, allowing 5-HT to persist in the synaptic cleft
What is the role of the prefrontal cortex and limbic system in executive control of food intake?
The prefrontal cortex: influences food-seeking behaviour
Integrates sensory information from inside and outside the body e.g. the smell of food
Receives emotional and cognitive information from the limbic system e.g. how do you feel about the food
Helps one make choices by translating all of the homeostatic and environmental information into adaptive behavioural response
Limbic system: complex system of nerves and networks in the brain; areas concerned with instinct, learning, reproductive behaviour; emotions/mood, pleasure (fear, anger, etc.)
The satiation of feeding behaviour is associated with motor planning and execution
Overall, the cortico-limbic mechanisms of reward are under executive control
What other inputs control feeding behaviour?
Orexigenic and anorexigenic neurotransmitters have been found in the hypothalamus Orexigenic neurotransmitters (e.g. NPY) increase appetite Anorexigenic neurotransmitters (e.g. CCK) decrease appetite
How do signals from the periphery and CNS control food intake?
Higher functions modulate responses to both CNS and peripheral cues (e.g. gut; environment) -> inhibition or stimulation of food intake
Factors that affect if food is sought or not and the type we ingest:
Food preferences
Emotions; psychological; physiological
Environment
Life style
Circadian rhythm- limits food intake to certain times (in some people)
Individual-based requirements (e.g. neural, metabolic and hormonal) may alter feeding behaviour
What signals out appetite?
[glucose]blood: stimulates gluco-receptors in hypothalamus
Brain has glucostat (like a glucose thermostat):
Decreases [glucose]blood -> induces hunger
Increases [glucose]blood -> induces satiety
Q-Why do diabetic patients feel hungry despite ↑[glucose]blood?
A-The blood glucose is not being taken up, they do not have the receptors required
Cold environments stimulate feeding while hot environments inhibit appetite
Afferent input:
Distension of a full stomach inhibits appetite; contraction of an empty stomach stimulates appetite
But this is not the case for everybody because some people binge eat
