Control of Food Intake

Question 1

State some factors that contribute to a sense of fullness

Answer 1

• VIP and NO are both important in the sense of fullness (satiety factors) - they allow accommodation of food intake within the stomach to occur
• Peptide YY is also important to allow accommodation to occur
• They are satiety factors as they decrease gut motility - the stomach is not emptied so the sense of fullness is reached

Question 2

State some factors involved in emptying of the stomach

Answer 2

• Involved in hunger
• Ghrelin is an important hormone involved in this process (hunger factor)
• Once the stomach has been emptied the feeling of hunger begins

Question 3

Describe how the stomach accommodates food after intake

Answer 3

• When food is consumed there is mechanical stimulation of the pharynx which leads to receptive relaxation
• The receptive relaxation signals the vagal centres in the brain which then sends signals to the stomach to allow adaptive relaxation via signals passed along the inhibitory vagal fibres which release acetylcholine to activate inhibitory enteric pathways
• Important factors - NO (nitric oxide) and VIP (vasoactive intestinal peptide) are then released by enteric pathways to relax the stomach muscle
• If the food consumed has a certain composition ie if it has a high lipid content then it causes a feedback relaxation of the stomach - relaxation is needed to allow bile to enter the stomach to emulsify the lipids following release of CCK (cholecystokinin)
• When food is in the duodenum it is unable to accommodate more food so sends signals to the stomach to relax (distension) to bring about a sense of fullness

Question 4

Describe what a vagotomy is and the effect it can have and why this effect is quite rare

Answer 4

• A vagotomy is the prevention of vagal nerve signals being sent by removal or severing of vagal nerves
• Vagotomy reduces accommodation and gastric compliance in 5% of cases
• Though denervation of intestines and stomach may have no effect on food intake due to signals from the pancreas, adipocytes, GI tract and CNS

Question 5

State the definitions of hunger, appetite and satiety

Answer 5

• Hunger - discomfort caused by a lack of food and the desire to eat - a strong physiological craving/drive for food/sensation of emptiness in the stomach
• Appetite - psychological drive/desire to satisfy the body’s needs of food - a hunger stimulated response - influenced by many factors such as family gatherings, food palatability, emotional habitual and circadian factors

*Satiety - state of being full after eating food

Question 6

State what aphagia and hyperphagia/polyphagia are

Answer 6

• Aphagia - inability or refusal to swallow
• Hyperphagia/polyphagia - an abnormal desire for food (extreme unsatisfied drive to eat)

Question 7

Describe how hunger, satiation and satiety are cues for starting and stopping eating

Answer 7

• Once you have eaten and are full the feeling of satiation tells you to stop eating
• Between meals satiety is a satisfaction that remains between meals
• As hunger begins to develop and grow the feeling of hunger tells you to start eating

Question 8

What part of the central nervous system controls food intake

Answer 8

Hypothalamus - it is a balance between stimulating and inhibiting forces in the hypothalamus which regulates feeding

Question 9

What are the reasons for differences in BMI?

Answer 9

• Genetic (70%)
• How much we eat and the composition of the food consumed

Question 10

Describe diurnal variation in food metabolism

Answer 10

• Carbohydrates are metabolised during the day
• Fats are metabolised at night
• The hypothalamus responds to the switch between carbohydrates and fats metabolism

Question 11

Describe the 7 components linked to the hypothalamus which exert control over food intake

Answer 11

1. Satiety centre -
   - The ventromedial nuclei of the hypothalamus (wall of the paraventricular nuclei)
   - Lesions of the ventromedial nuclei causes hyperphagia which increases appetite and can lead to excessive hunger which precedes weight gain
2. Feeding/hunger/thirst centre -
   - Lateral nuclei of the hypothalamus
   - Stimulation of the lateral hypothalamus increasing how often a person feeds
   - A lesion in this region can lead to aphasia meaning an inability or reluctance to swallow which leads to weight loss
3. Dorsomedial nucleus -
   - Modulates energy intake - release of neuropeptide Y into the dorsomedial nucleus leads to increased feeding
4. Paraventricular nucleus -
   - Modulates feeding behaviours - neuropeptide Y and opioids can increase feeding while leptin can decrease food intake
5. Arcuate nucleus -
   - Its neurons produce orexigenic signals (neuropeptide Y, opioids, dynorphin, beta endorphin, galanin and glutamate which increase feeding
6. Suprachiasmatic nucleus -
   - Controls our perception of the light dark cycle and so influences circadian rhythms - how we perceive this and our sleep wake cycles can influence our appetites and so cause us to eat at certain times
7. Medial amygdaloid nucleus -
   - A subregion of the amygdaloid complex - a role in feeding behaviour and participation in regulation of food intake has been proposed
   - Particular ligands such as 5-HT have been shown to regulate appetite/food intake by binding to the medial amygdaloid nucleus

Question 12

State some other factors that can control feeding behaviours

Answer 12

• Orexigenic/anorexigenic neurotransmitters have been found in the hypothalamus
• Orexigenic neurotransmitters increase appetite
• Anorexigenic neurotransmitters decrease appetite
• The orexigenic and anorexigenic neurotransmitters modulate feeding behaviour by binding to the hypothalamic nuclei

Question 13

Describe what zimelidine does

Answer 13

Inhibits the reuptake of 5-HT from the synaptic cleft allowing 5-HT to persist in it

It is therefore considered an anorexigenic factor as it decreases appetite

Question 14

State the role of the prefrontal cortex in control of food intake

Answer 14

• Integrates sensory information from inside and outside the body
• Receives emotional and cognitive information from the limbic system
• Helps a person to make choice about eating by translating all of the homeostatic and environmental information into behavioural responses

Question 15

State the role of the limbic system in control of food intake

Answer 15

• Complex system of nerves and networks in the brain
• Areas concerned with instinct, learning, reproductive behaviour, emotions/mood, pleasure
• The act of satiation of feeding behaviour is associated with motor planning and execution
• Overall the cortico limbic mechanisms of reward are under executive control

Question 16

State some factors that impact if we sought after food and the type of food we ingest

Answer 16

• Food preferences
• Emotions, psychological, physiological
• Environment
• Lifestyle
• In some people circadian rhythms limit food intake to certain times
• Individual based requirements - e.g. neural, metabolic and hormonal may alter feeding behaviour

Question 17

State what signals our appetite in terms of glucose

Answer 17

• The [glucose] in the blood stimulates gluco-receptors in the hypothalamus
• The brain has a glucostat - if the [glucose] in the blood decreases then it induces hunger, if the [glucose] in the blood increases then it induces satiety

Question 18

Why does a diabetic patient still feel hungry despite a high [glucose] in the blood

Answer 18

Because they cannot take up that blood glucose

Question 19

How does temperature impact appetite

Answer 19

Cold environments also stimulate feeding while hot environments inhibits appetite

Question 20

Describe the role of insulin in control of food intake

Answer 20

• Insulin decreases food intake
• The insulin released depends on the white adipose tissue presence
• The more adipose tissue there is the more signals are sent to the pancreas and the more insulin is released from beta cells
• The insulin travels in the bloodstream and will enter brain capillary where it will interact with certain nuclei to cause catabolic or anabolic effects
• Inhibitory effects at NPY/AgRP neurons these neurons usually stimulate appetite - catabolic effects - reduce food intake reduces body fat
• Stimulatory effects at POMC/CART neurons - also usually reduce food intake/appetite when stimulated
• Once there has been a reduction in food intake and blood [insulin] have reduced then the brain centres have anabolic effects - increased food intake increases body fat
• Thus there is modulation of energy homeostasis

Question 21

Describe the role of glucagon in control of food intake

Answer 21

• Released from alpha cells in the pancreas
• It can increase the secretion of glucose by promoting glucagon -> glucose conversion
• The release of glucagon during feeding leads to a feeling of satiety

Question 22

Describe the role of CCK (a gut hormone) in food intake control

Answer 22

• Fat ingestion causes CCK release and the slowing of gastric emptying causing a sense of fullness
• This is because fat is released in response to fat in the duodenum which needs to be emulsified by action of bile acids - during this time no more food enters the duodenum so receptive relaxation of the stomach occurs
• CCK from I cells in the intestine or nerve endings and somatostatin are satiety factors which inhibit further food intake
• Injection of CCK into the brain has been shown to reduce appetite so may have a use in treating obesity

Question 23

Describe the role of leptin in control of food intake

Answer 23

• Fat cells secrete leptin (16 kDa protein) which is from a gene expressed mainly in adipocytes
• Controls fat stores by operating a feedback mechanism between adipose tissue and the brain
• There is a high correlation of leptin levels with body fat in humans and animals p- the larger the size of the adipose tissue the greater the leptin secreted by adipose tissue
• Administration of leptin can decrease food intake induce weight loss and increase energy expenditure
• Leptin acts on the hypothalamus in order to change food intake
• It increases the expression of anorexigenic factors e.g. proopiomelanocortin (POMC), cocaine and amphetamine regulated transcript (CART), and corticotropin releasing hormone (CRH)
• It also inhibited neuropeptide Y which usually stimulates feeding

Question 24

Describe what leptin resistance can lead to

Answer 24

May lead to binge eating despite obesity

Hyperphagia and severe obesity occurs in humans with leptin deficiencies or leptin receptor defects

Question 25

Describe the role of ghrelin in control of food intake

Answer 25

• An appetite inducing hormone which stimulates hunger
• Fast acting to stimulate food intake
• Released by the stomach, pancreas, and adrenals in response to nutritional status
• Increases central orexins e.g. NPY and AgRP which are hunger signals - circulating levels of ghrelin increase pre meal and decrease post meal (pre and post prandial)

Question 26

Describe the interrelationship between leptin and ghrelin

Answer 26

• Leptin can inhibit the secretion of ghrelin
• Ghrelin suppresses the ability of leptin to stimulate anorexigenic factors
• Leptin and ghrelin act reciprocally on food intake - stimulation of their receptors in the hypothalamus change food intake

Question 27

Describe the role of obestatin in control of food intake

Answer 27

• Produced by the epithelial cells of the stomach
• Encoded by the ghrelin gene but it opposes the effects of ghrelin on food intake
• Suppresses food intake and so decreases body weight gain
• Antagonises ghrelin induced food intake and growth hormone secretion
• Obestatin mediates its effects via different receptors to ghrelin