Control of Food Intake Flashcards
Key definitions
satiety appetite hunger aphagia hyperphagia/polyphagia
- 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)
why is there no voluntary control with storage of food
ANS = storage of food in the stomach WITHOUT voluntary control
What happens to stomach in fasting state?
what chnages when food enters?
what happens when we are full?
what will relaxtions and contractions lead to?
- Fasting state: Stomach = small volume.
- Presence of food = accommodation to occur (VIP and NO IMPORTANT HERE).
- When full = satiety -> short term // long term depending on how full we are.
- Relaxations//contractions -> will empty the stomach = feel hunger (stimulated by GHRELIN).
Main Control of Food Intake?
how does weight change with age?
what are 2 reasons for differences in BMI?
Main control = hypothalamic control
Young people = maintain a constant body weight, BUT decreases with age (middle aged spread)
Reasons for differences in BMI
o Genes
o How much we eat and its consumption
Accommodation of Food
what are the three types of relaxtion? How do they turn on or come about?
what is vagotomy? what does it do? why do patients get early satiety? why does it do this?
3 types of relaxation:
- Receptive relaxation
o Mechanical stimuli IN PHARYNX -> sent to the vagal nerve. - Vagal reflex = relaxation to occur via INHIBITORY VAGAL FIBRES = release NO and VIP.
- Adaptive relaxation
o Food in stomach = adaptation. Further felt by TENSION RECEPTORS -> furthers relaxation.
Vagotomy
- Vagotomy impairs accommodation // emptying -> early satiety in some patients.
- Caused by disturbance to fundic tone -> ↓contractility -> stasis and bloating.
- Vagotomy ↓ accommodation // gastric compliance.
Hypothalamic control
how does hunger, satiation and satiety help us?
where in the hypothalamus is this control? what do they control?
2 other inputs that control feeding behaviour?
Hunger, satiation, and satiety = cues -> tell you when to start and stop eating.
- Hunger -> START EATNG -> satiation -> STOP EATING -> Hunger
Base of the hypothalamus = several nuclei = regulate energy homeostasis//controlling appetite //size of portions // ingestive behaviour.
Other inputs = control feeding behaviour:
• Orexigenic neurotransmitters: ↑appetite
• Anorexigenic neurotransmitters: ↓ appetite
Relaxation of the reservoir (fundus) is mediated by reflexes and can be differentiated into 3 types
name one component mediator: name these
What mediate these reflexes?
receptive (mechanical stimulation of pharynx – mechanoreceptors, sight),
adaptive (vagal innervation (NO/VIP), tension of stomach)
feedback (nutrients, CCK).
mediated by non-adrenergic, non-cholinergic (NANC) mechanisms (i.e., inhibition involving NO, VIP, etc.) as well as by reflex chains involving release of noradrenaline.
Summary of factors that influence food intake
3 key categories? name a few things for these
External factors- e.g., food availability, variety of food available, social eating, daily routines.
Emotional state - stress, anxiety, depression.
Physiological regulation
Feeding behaviour/food intake = modulated by: Hypothalamic nuclei
Name them
hunger centre?
satiety centre? what does it work with? how can this go wrong?
energy intake - hunger centre? what does it release and effect?
modulates feeding bahaviour? what does it work with? what is their effect? what is released and their effects?
orexigenic signals? what is released?
mood to drive to eat? what does it control? what may alter feeding behaviour?
last nucleus? where is it? what does it regulate and via what?
Hypothalamic nuclei
• Lateral hypothalamus (LH) = hunger centre
o Hypothalamus = hunger
• Ventromedial nucleus (VMN) = satiety centre
o Works with the LH to restrain/promote feeding
o Ability to restrain feeding if required; lesion -> ↑ appetite, with persist weight gain
• Dorsomedial nucleus (DMN) = Energy intake (hunger centre)
o Release Neuropeptide Y into DMN -> ↑ feeding
• Paraventricular nucleus (PVN) = modulates feeding behaviour
o Works in conjunction with the perifornical hypothalamus
o Control feeding behaviour
o NPY, opioids, GABA, etc. -> ↑ feeding leptin ->↓ food intake
• Arcuate nucleus
o Neurons -> orexigenic signals (NPY, the opioids, dynorphin, β-endorphin, POMC, galanin, amino acids, GABA and glutamate)
• Suprachiasmatic nucleus
o Appetite or the sensation of hunger → mood/drive to eat
o Perception of the light-dark cycle (circadian rhythms) = human body clock
o Individual-based requirements (e.g., neural, metabolic, and hormonal) may alter feeding behaviour
• Medial amygdaloid nucleus
o It is a sub-region of the amygdaloid complex
o Regulation of food intake
o 5-HT (via 5-HT2C and 5-HT1A): regulates appetite and food intake
Regulation of appetite in the hypothalamus by 5-HT2C agonist
What is released to stimulate appetite?
what is released to suppress appetite? what is the precursor to this molecule? what receptor does it bind to?
Name a agonist to regulate appetite? where does it bind and where is this located?
How can the appetite stimulating pathway stimulate appetite?
What is zimelidine?
what happens when you give zimelidine to fasted and fed rats? how does it change with conc?
On side A, the appetite suppressing pathway is not stimulated (POMC neuron) because there is no 5-HT2C agonist released into the environment.
This means that it does not bind to its receptor (MC4R) so that receptor is free.
The appetite stimulating pathway is stimulated releasing neurotransmitters = NPY // AgRP and receptor is free -> ↑ appeitite.
On side B, there is an agonist (mCPP) which can bind to its receptor. (5-HT2C)
This stimulates the POMC neuron.
POMC is active -> metabolised to αMSH -> gets secreted it binds to MC4R = decreased appetite.
Zimelidine is a drug – a 5-HT2C neuronal uptake inhibitor and allows it to persist in the synaptic cleft.
- If you expose rats to 5-HT and keep some of them fasted and then feed the rest while also exposing to different concentrations of zimelidine (dissolved in αCSF) – the fed rats have decreased food intake generally.
- With the fasted rats, there is a pattern – higher concentrations of zimelidine leads to decreased food intake. This is because the drug promotes decreased appetite.
Central control of food intake
Name some anorexigenic factors
what is the Diurnal variation in food intake?
Anorexigenic factors
5-HT (5-HT2C and 5-HT1A), dopamine, GABA →↓ appetite
Diurnal variation in food intake
- Carbohydrates metabolised during the day
- Fats metabolised at night
- Hypothalamus responds to the switch between carbohydrate and fat metabolism
Executive control of food intake
Name the 2 main systems
which one is to do with instinct and mood? which one inetgrates sensory info? hwo are they connected? what do they do?
Prefrontal cortex
The prefrontal cortex = integration of sensory information from inside and outside the body. It receives emotional and cognitive information from the limbic system.
Helps make choices by translating all of the homeostatic and environmental information into adaptive behavioural response.
Limbic system
The limbic system = complex system of nerves and networks in the brain; areas concerned with instinct and mood. It may control emotions, pleasure (fear, anger, etc.).
So cortico-limbic mechanisms of reward appear to be under executive control – they can be modulated to some extent depending on how hungry one is. The satiation of feeding behaviour is associated with motor planning and execution
Control of food intake: integration of many signals
what nerves tell the brain how much we have eaten and when to stop eating?
what part of the hypothalamus modulates energy intake? what if this was destroyed? what three molecules will stimulate appetite? what are these molecules called?
from where does this area recieve projections from? what neurones? what cells does it have?
what is a very sensitive area for NPY-induced eating? at what levels is NPY found? what if NPY was injected to hypothalamus?
What is the c-shaped bundle of nerve fibres in the brain? where does it carry nerves from and to where? what is this part of the brain involved in?
What is the hunger or feadding centre?
what is the satiety centre?
which part of the brain releases regulatory hormones? what is this integral to? where is this?
Where is arc?
- Stomach nerves are responsible for telling the brain how much food a person has eaten, and when to stop eating.
- DMN - dorsomedial nucleus – modulates energy intake; its destruction → hyperphagia & obesity; injection of GABA, NPY, galanin (orexigenic agents) stimulates appetite/food intake.
- DMN also receive projections from agRP/NPY neurons from ARC; it also has NPY-expressing cells.
- PFA = perifornical area – a very sensitive hypothalamic site for NPY-induced eating; NPY is found in high concentrations within neurons of hypothalamus – if injected into the hypothalamus, it stimulates powerful stimulus to eat.
- FX: C-shaped bundle of nerve fibres in the brain that carries signals from the hippocampus to the mammillary bodies (- are a pair of small round bodies, located on the under surface of the brain that, as part of the diencephalon, form part of the limbic system; it is for re-collective memory) and then to the anterior nuclei of thalamus. It is part of the limbic system – involved in memory and recall therfore carries signals; re-collective memory (remember what that food tastes like and could decide to have it again or not; but of course, we are also sometimes adventurous – try new things).
- LHA: lateral hypothalamic area = hunger or feeding centre.
- VMN = ventromedial nucleus = satiety centre.
- ME: median eminence - part of the hypothalamus from which regulatory hormones are released; integral to the hypophyseal portal system
- ARC: arcuate nucleus, also called infundibular nucleus= aggregation of neurons in the medio-basal hypothalamus.
Central control of food intake: where is the switch?
where is the satiety centre?
what will stimulation and lesions cause?
Where is the feeding centre?
what will stimulation and lesions cause?
What do opiods and ghr do for appepite? how?
what is the hedonic system?
What is the glucostat? what does it do?
REMEMBER that the satiety centre is part of the hypothalamus and the ventromedial wall of paraventricular nucleus. Stimulation of ventromedial wall of paraventricular nucleus → aphagia. Lesions of ventromedial wall of paraventricular nucleus → hyperphagia (increased appetite or excessive hunger).
REMEMBER that the feeding centre is part of the lateral hypothalamus. Stimulation of lateral hypothalamus → ↑ feeding. Lesion of this region → aphagia.
The brain has a glucostat that measures the amount of glucose that reaches it. This is because the brain heavily relies on glucose to function.
Opioids, growth hormone releasing hormone →↑ appetite. It is argued that opioid receptor agonism generally enhances food intake by increasing the positive hedonic valence of food, while opioid receptor antagonism reduces or blocks this effective response.
Control of food intake
what modulate resposnes to both cna and peripheral cues?
Factors that affect if food is sought or not and the type we ingest
how does circadian rhythmn affect food intake?
Signals from periphery and CNS control nutrient intake
Higher functions modulate responses to both CNS and peripheral cues → inhibition or stimulation of intake
Factors that affect if food is sought or not and the type we ingest: Food preferences Emotions Environment Life style
Circadian rhythm – limits food intake to certain times (in some people)
-> Stomach nerves ‘act as a clock’ to coordinate food intake - The activity of stomach nerves has a circadian rhythm, which may limit our food intake to certain times throughout the day
