26) Control of food intake Flashcards
1
Q
How is the storage of food in the stomach accommodated?
A
- The ANS enables the storage of food in the stomach.
- All we have to do is eat and the stomach accommodates the food
2
Q
What happens in the stomach during fasting?
A
- During the fasting state the stomach is contracted
3
Q
What happens in the stomach during consumption?
A
- When the food is in the mouth it is known as receptive relaxation. This receptive relaxation is communicated to the vagus centre in the higher centres of the brain.
- As a result messages are sent along the inhibitory vagal fibre to the stomach to allow adaptive relaxation to occur
- Vasoactive Intestinal Peptide (VIP) and Nitric oxide (NO) allow accommodation to occur and are known as satiety factors
- PYY is also a satiety factor which decreases gut motility which means the stomach is not emptied so satiety/fullness is achieved
- As the food makes its way into the small intestines there is a feedback reaction occurring depending on the contents of the food
4
Q
What happens in the stomach during emptying?
A
- During emptying a hunger fact (called ghrelin) is released causing emptying
- Emptying of the stomach causes us to feel hunger
5
Q
What is adaptive relaxation?
A
- The presence of food in the stomach that allows accommodation to occur causing a sense of fullness (satiety)
6
Q
What happens when lipids enter the small intestine?
A
- A feedback mechanism is mounted which informs the higher centres of the brain to release bile for the emulsification of the lipids.
- There is a release of CCK which causes the secretion of bile
- This allows lipase to works on emulsified lipids
- During this time no more food is allowed to pass through and hence the stomach relaxes
- This relaxed state of the stomach causes a state of fullness (satiety)
7
Q
Why can the stomach respond to stimuli?
A
- The stomach is encircled by a lot of nerves which allow the stomach to respond to stimuli within the lumen of the gut
- The greater curvature of the stomach contains pacemaker cells which allow contractions to occur by initiating electrical impulses
- When the vagus nerve in the stomach is stimulated we end up with a vagovagal reflex which allow the food to be moved along the GI tract
8
Q
What is vagotomy?
A
- A surgical operation in which one or more branches of the vagus nerve are cut
9
Q
What is the effect of vagotomy on the stomach?
A
- Vagotomy impairs accommodation and emptying as we loose the pacemaker cells found on the greater curvature of the stomach.
- As a result it interferes with the vagovagal reflex which means there are less contractions pushing the food through.
- Hence the food is unable to be moved out of the stomach and causes early satiety in some patients
10
Q
What is the effect of denervation of intestines and stomach?
A
- There may be no effect on food intake as there may be other tissues and organs which release other factors that can mediate other effects (i.e. hunger)
- These signals/factors can come from the pancreas, adipocytes, GIT and CNS
11
Q
What is hunger?
A
- A state of discomfort caused by lack of food and desire to eat. It can be a strong physiological craving or drive for food
12
Q
What is appetite?
A
- A physiological desire/drive to staisfy the body’s need for food
- It is stimulated by hunger
13
Q
What is satiety?
A
- The state of being “full” after eating food. There is no longer the urge to continue eating
14
Q
What is aphagia?
A
- The inability or refusal to swallow
15
Q
What is hyperphagia/polyphagia?
A
- An abnormal desire for food (an extreme unsatisfied drive to eat)
16
Q
What factors influence appetite?
A
- Family gatherings (e.g. during Christmas times)
- Emotional
- Food palatability (the way it is presented)
- Circadian (body clock)
- Habitual
- Cardiac rhythm
- Individual-based requirement (e.g. neural, metabolic and hormonal)
17
Q
How do we know when to start/stop eating?
A
- Hunger, satiation and satiety are cues which tell our body when to start eating and when to stop
- Hunger tells us to start eating until we get full
- Satiation tells us to stop eating when we are full
- Satiety is the satisfaction between meals where we start to get hungry again
- This forms a cycle of:
Hunger –> Satiation –> Satiety —> Hunger
18
Q
How is food intake controlled?
A
- Signals from the CNS and periphery control nutrient uptake
- There is a balance of stimulating and inhibiting forces in the hypothalamus which regulates feeding
- There are several nuclei located at the base of the hypothalamus which regulate energy homeostasis and control appetite
- There is also a diurnal variation in food metabolism. Carbohydrate metabolism occurs during the day while fats are metabolised in the night. The hypothalamus has to respond to switch between carbohydrate and fat metabolism
19
Q
What are the reasons for differences in BMI?
A
- Genes
- How much we eat and its composition
20
Q
What are the different nuclei of the hypothalamus that control food intake?
A
- Lateral hypothalamic nuclei
- Ventromedial nuclei
- Dorsomedial nuclei (DSN)
- Paraventricular nucleus (PVN)
- Arcuate nuclei
- Suprachiasmatic nucleus
- Medial amygdaloid nucleus
21
Q
What is the function of the ventromedial nuclei?
A
- The satiety centre found in the hypothalamus and is important to satisfy our desire for food
- Stimulation of ventromedial nuclei leads to aphagia (swallowing difficulties) as we feel a sense of fullness
- Lesions/destruction of the ventromedial nuclei leads to hyperphagia (increased appetite or excessive hunger) causing weight gain
22
Q
What is the function of the lateral hypothalamic nuclei?
A
- The feeding/hunger/thirst centre
- Stimulation of the lateral hypothalamic nuclei leads to increased feeding
- Lesions/destruction of the lateral hypothalamic nuclei can lead to aphagia
23
Q
What are the experimental data of the effect of lesions on food consumption in cats?
A
- When a ventromedial hypothalamic lesion is carried out the cat starts to gain weight as it suffers from hyperphagia
- When the lateral hypothalamic lesion is carried out the cat starts to loose weight as it suffers from loss of appetite
24
Q
What neurotransmitters control feeding behaviour?
A
- Orexigenic and anorexigenic neurotransmitters are found in the hypothalamus
- They modulate feeding behaviour by binding to hypothalamic nuclei
- Orexigenic neurotransmitters increase appetite
- Anorexigenic neurotransmitters decrease appetite
25
Q
What is the function of the Dorsomedial nucleus (DMN)?
A
- There is a release of neuropeptide Y (NPY) into the dorsomedial nucleus which increases feeding
- In doing so it modulates energy intake/homeostasis
- It is also called the hunger centre
26
Q
What is the function of the paraventricular nucleus (PVN)?
A
- Works with the perifornical hypothalamus to control feeding behaviour
- They secrete neuropeptide Y (NPY) which increase feeding
- Leptin (a factor released by fat) acts on the paraventricular nucleus to decrease food intake
- Opioids can interact with the PVN to increase feeding and food intake
27
Q
What is the function of the Arcuate nucleus?
A
- It contains neurones which produce orexigenic signals (e.g. NPY, opioids, dynorhin, Beta-endorphins, galanin, glutamate) which increase feeding
28
Q
What is the function of the Suprachiasmatic nucleus?
A
- It is where the human body clock is located and influences appetite or the drive to eat
- It involves the perception of light-dark cycles
29
Q
What is the function of the Medial amygdaloid nucleus?
A
- It is a sub-region of the amygdaloid complex.
- It is proposed that it participates in the regulation of food intake
- This is because scientists have noticed that it interacts with specific ligands (e.g. 5-HT) and modulate feeding behaviour
30
Q
What is 5-HT?
A
- An anorexigenic factor that interacts with the amygdaloid nucleus which decreases appetite
31
Q
What is zimelidine?
A
- A drug that inhibits the reuptake of 5-HT from the synaptic cleft allowing it to persist within the cleft
- As a result it will cause a persistent decreased appetite from normal causing a decrease in overall food consumption
32
Q
How does the prefrontal cortex and limbic system control food seeking behaviour?
A
- The prefrontal cortex integrates sensory information from inside and outside the body
- It receives emotional and cognitive information from the limbic system
- Helps to make a choice by translating all the information into a behavioural (adaptive) response
- The limbic system is a complex system of nerves in the brain.
- This area is associated with learning, instinct, reproductive behaviour, emotions and pleasure (e.g. fear, anger, etc)
- The act of satiation is associated with motor planning and execution. I.e. in order to satisfy your hunger you have to execute the process by moving to the food and swallowing
- Overall it is the cortico-limbic mechanism that rewards seeking food and executing the act of eating and satisfying our desire to be full
33
Q
What factors affect the type of food we ingest?
A
- Food preferences
- Emotions (physiological and psychological)
- Environment
- Lifestyle
34
Q
How does glucose influence appetite?
A
- Glucose in the blood stimulates gluco-receptors in the hypothalamus
- A decrease of glucose in the blood causes hunger
- An increase of glucose in the blood causes satiety
35
Q
Why do diabetic people feel hungry despite a high concentration of glucose in the blood?
A
- The blood glucose is not taken up
36
Q
How does temperature affect appetite?
A
- Cold environments stimulate feeding while hot environment inhibit appetite
37
Q
How does insulin influence food intake?
A
- Insulin decreases food intake
- The amount of insulin produced is dependent on white adipose (fat) tissue which communicates with the pancreas to secrete insulin
- This insulin travels through brain capillaries where it can interact with brain nuclei to have two possible effects. It can inhibit neurones that stimulate appetite or a stimulate neurones that decrease appetite.
- As a result we can have two possible outputs: Catabolic and anabolic
- Catabolic: reduction of food intake causing a decrease in body fat (which in turn reduces insulin produced) causing the inhibitory effect
- Anabolic: increased food intake causing an increase body fat (which in turn will increase insulin produced) causing the stimulatory effect
38
Q
How does glucagon influence food intake?
A
- Glucagon can either affect the brain directly or via the liver through insulin
- It increases glucose secretions and as a result decreases food intake
39
Q
How do gut hormones influence food intake?
A
- When fat is ingested it reaches the duodenum and causes CCK release
- CCK causes the contraction of the gall bladder leading to the secretion of bile to help emulsify fats.
- During emulsification in the duodenum more food cannot enter the duodenum.
- A message is sent to the gut which promotes receptive relaxation causing satiety (sense of fullness)
- This means CCK is a satiety signal which reduces appetite and inhibits further food intake
40
Q
What can CCK be used to treat?
A
- CCK derivatives are potential medicine used to treat obesity
41
Q
How does Leptin control food intake?
A
- Adipocytes (fat cells) secrete Leptin
- It controls fat stores by operating a feedback mechanism between adipose tissue and the hypothalamus.
- It increases the expression of anorexigenic factors (e.g. CART) and inhibits orexigenic factors (e.g. NPY)
- The larger the size of the adipose tissue the greater the leptin secreted by the adipose tissue.
42
Q
What can leptin resistance cause?
A
- This is because there is no leptin being produced so there is no signalling sent to the brain and so food intake cannot change
- It causes hyperphagia and severe obesity and may even lead to binge eating
43
Q
How can leptin be used in pharmaceutical drugs?
A
- Administration of leptin can decrease food intake.
- This is because as we increase leptin it sends signals to the brain to prevent food intake
- As a result this induces weight loss and also increases energy expenditure
44
Q
How does ghrelin affect food intake?
A
- It is an appetite inducing hormone which stimulates hunger by increasing central orexins (hunger signals) such as NPY
- It is fast acting and stimulates food intake
- It is released by the stomach, pancreas and adrenals in response to nutritional status
- Before a meal (pre-prandial) circulating levels of ghrelin increase and after a meal (post-prandial) circulating levels of ghrelin decrease
45
Q
How do Leptin and Ghrelin interact?
A
- Leptin and ghrelin act reciprocally on food intake
- Stimulation of their receptors in the hypothalamus can lead to changes in food intake
- Leptin can inhibit the secretion of ghrelin
- Ghrelin supresses the ability of leptin to stimulate anorexigenic factors
46
Q
How does Obestatin control food intake?
A
- They are produced by epithelial cells of the stomach
- They are encoded by ghrelin genes however it opposes the effect of ghrelin on food intake
- It supresses food intake by supressing appetite and as a result there is a decrease in weight gain in a person
- It also antagonises ghrelin induced food intake and growth hormone
- Obestatin interacts with different receptors from ghrelin
