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Gastrointestinal > Control of Food Intake > Flashcards

Control of Food Intake Flashcards

1
Q

What enables food to be stored in the stomach?

A

The autonomic nervous system enables involuntary food storage in the stomach

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2
Q

What is the role of the ANS?

A

ANS controls bodily functions unconsciously

e.g. breathing, heartbeat and digestive processes

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3
Q

What is satiety?

A

When food is present in the gut - full sensation

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4
Q

What is stomach emptying?

A

Elicits hunger

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5
Q

What controls gut motility and accommodation?

A

There are factors present in the gut that are important in the control of gut accommodation and motility / emptying ∴ energy fluxes

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6
Q

What is the role of ghrelin?

A

Secreted by fundus
Increases sense of hunger stimulating gastric emptying
- stimulates NPY and AgRP

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7
Q

What is the role of PYY?

A

Opposes ghrelin

signals satiety, inhibits gut motility / emptying

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8
Q

What is the role of amylin?

A

Helps reduce food intake through medulla of brain stem by delaying gastric emptying

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9
Q

What is an enterogastrone?

A

Hormones secreted by duodenum mucosa in response to dietary lipids
- inhibit aboral motion of chyme

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10
Q

Name some enterogastrones

A

CCK (cholecystokinin)
GIP (gastric inhibitory peptide)
secretin

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11
Q

What regulates gastric relaxation?

A

The relaxation of the gastric reservoir is regulated mainly by reflexes

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12
Q

How is gastric reservoir relaxed?

A 
Inhibitory vagal fibres release ACh 
Activating inhibitory anteric pathways that release:
- NO
- VIP
- PACAP
- and/or ATP

in order to relax muscle

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13
Q

What are the 3 types of relaxation that occur in the gastric reservoir (stomach)?

A
  1. Receptive relaxation
  2. Adaptive relaxation
  3. Feedback relaxation
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14
Q

What stimulates receptive relaxation?

A

Mechanical stimulation of pharynx via mechanoceptors / sight

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15
Q

What causes adaptive relaxation?

A

Vagal innervation via NO / VIP

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16
Q

What stimulates feedback relaxation?

A

Nutrients and enterogastrones (CCK)

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17
Q

What regulates the relaxation mechanisms of the stomach?

A

The receptive, adaptive and feedback relaxation of the stomach are mediated by NANC mechanisms (e.g. NO / VIP, PACAP etc.) and by reflex chains including the release of NA

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18
Q

What is PACAP?

A

pituitary adenylate cyclase - activating peptide

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19
Q

Where is PACAP found in the body?

A

isolated from the pituitary -> stimulates AC in anterior pituitary

High levels in the brain and gut
- myenteric and submucosal ganglia

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20
Q

What is the function of PACAP?

A

Mediates neuronal regulation of gastric acid secretion and intestinal motility

Stimulates relaxation of colonic smooth muscle

Stimulates pancreatic secretions; insulin + glucagon

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21
Q

What is a vagotomy?

A

Surgical procedure involving the removal of part of the vagus nerve

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22
Q

What is the effect of a vagotomy?

A

Vagotomy impairs:

  • accommodation
  • gastric compliance
  • emptying

can be a cause of early satiety in some patients

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23
Q

What causes gastroparesis?

A

Prior gastric surgery

Non motor factors may also be involved as symptoms don’t always correlate with delays in gastric emptying

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24
Q

What is gastroparesis?

A

Delayed gastric emptying

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25
Q

What is gastric compliance?

A

Accommodation and perception of gastric distension

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26
Q

What effect will a vagotomy have on gastric compliance?

A

Denervation will have little to no effect; Peripheral signals from adrenals
The pancreas, adipose tissue, GIT and CNS will continue to operate to control food intake and energy expenditure

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27
Q

What is hunger?

A

Discomfort caused by a lack of food and desire to eat

A strong physical craving for food / sensation of emptiness in the stomach

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28
Q

What is appetite?

A

A psychological desire / drive to satisfy body’s need for food (hunger stimulated response)

  • can have an appetite and not be hungry (+ vice versa)
  • due to stress or illness
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29
Q

What is satiety?

A

State of being full after eating food

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30
Q

What is Aphagia?

A

The inability / refusal to swallow

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31
Q

How do hunger and satiety work together?

A

Hunger and satiety are cues that tell you when to stop and start eating
Satiety signals prolong the interval until hunger or the onset of the next meal

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32
Q

What is hunger and satiety dependent upon?

A

Hypothalamic control and BMI (70% due to genes)

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33
Q

What is BMI?

A

Body mass index

each individual has a genetically determined weight + height set point

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34
Q

What regulates weight and BMI?

A

Body weight and BMI are tightly regulated by an energy homeostatic mechanism

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35
Q

What influences appetite?

A
  • family gatherings
  • food palatability
  • emotional
  • habitual
  • circadian rhythms
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36
Q

What role does the hypothalamus play in control of food intake?

A

Hypothalamus is the control centre of food intake and appetite
-> controls hunger and thirst

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37
Q

What enables the hypothalamus to carry out its functions?

A

The hypothalamus base contains several nuclei that regulate energy homeostasis
-> control appetite; size of helping + ingestive behaviour

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38
Q

Describe the features of the prefrontal cortex that aid its role in controlling food intake

A
  • ‘food seeking’
  • Integrates sensory info from inside and outside body
  • receives emotional + cognitive info from limbic system
  • intimately related to cortical areas involved in motor
    planning and execution
  • translates all homeostatic + environmental info into
    adaptive behavioural responses
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39
Q

What is the limbic system?

A

Complex system of nerves and networks in the brain

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40
Q

Where is the prefrontal cortex found?

A

Covers front part of frontal lobe in the brain

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41
Q

What is the role of the limbic system?

A
  • areas concerned with instinct and mood
  • controls emotions, fear, pleasure, anger, also drives
    hunger, sex, dominance, care of offspring etc.
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42
Q

Which hypothalamic nuclei are involved in modulating feeding behaviour?

A
  • Lateral hypothalamus (LH)
  • Ventromedial Nucleus (VMN)
  • Dorsomedial Nucleus (DMN)
  • Paraventricular Nucleus (PVN)
  • Accurate Nucleus
  • Suprachiasmatic Nucleus
43
Q

What is the specific role of the lateral hypothalamus?

A

LH is the hunger / thirst centre

44
Q

What is the role of the VMN?

A

Ventromedial nucleus is the satiety centre

45
Q

What is the significance of the LH and VMN?

A

LH and VMN both have the ability to restrain feeding if required
lesion of VMN leads to increased appetite, with weight gain that persists

46
Q

What is the function of the DMN?

A

Modulates energy intake
hunger centre
Releases NPY into DMN to increase feeding

47
Q

What is the function of the PVN?

A

Modulates feeding behaviour
PVN and perifornical hypothalamus control feeding behaviour
NPY, opioids, GABA etc. increase feeding
Leptin decreases food intake

48
Q

What is the function of the Accurate nucleus?

A

Neurons produce orexigenic signals:

  • NPY
  • opioids
  • dynorphin
  • ꞵ-endorphin
  • POMC
  • amino acids
  • GABA
  • glutamate
49
Q

What is the role of the Suprachiasmatic nucleus?

A

Location of human body clock - circadian rhythms control

  • perception of light-dark cycle
  • hunger / appetite sensation

individual based requirements (neuronal, hormonal, metabolic) may affect feeding behaviour

50
Q

What is the significance of the Serotonin 5-HT(2C) and 5-H(1A) receptors?

A

5-HT(2C) and 5-HT(1A) Serotonin ligand receptors are critical in the regulation of food intake

  • stimulate appetite
  • suppress appetite
51
Q

How do 5HT receptors stimulate appetite?

A

Appetite stimulating neurons release AgRP and NPY
MC4R isn’t occupied
-> so appetite is stimulated

52
Q

How do 5HT receptors suppress appetite?

A

Appetite suppressing neurons release POMC
POMC broken down into ꭤ-MSH
ꭤ-MSH binds to MC4R which suppress appetite

53
Q

What is mCPP?

A

meta-Chlorophenylpiperazine is a psychoactive drug that suppresses appetite

54
Q

Explain how mCPP suppresses appetite?

A
  1. mCPP binds to 5HT(2C) receptors on appetite
    suppressing POMC neurons
  2. Activates POMC neurons to release ꭤ-MSH
  3. ꭤ-MSH binds to MC4R to suppress appetite
55
Q

Describe the diurnal variation in food intake

A
  • Carbohydrates metabolised during the day
  • Fats metabolised at night
  • Hypothalamus responds to switch between
    carbohydrate and fat metabolism
56
Q

How does Zimeldine suppress appetite?

A

Inhibits the re-uptake of 5HT from the synaptic cleft

5HT persists and is able to mediate its effects in suppressing appetite

57
Q

What are the side effects of Zimeldine?

A
  • dry mouth
  • increased sweating
  • vertigo
  • nausea
58
Q

Where is the satiety centre located?

A

The ventromedial hypothalamus (VMN)

59
Q

What does the stimulation of VMN cause?

A

aphagia

60
Q

What is the effect of VMN lesions?

A

hyper-aphagia

61
Q

Where is the hunger centre in the body?

A

The lateral hypothalamus (LH)

62
Q

What is the effect of LH stimulation?

A

increased feeding

63
Q

What does lesions of LH cause?

A

aphagia

64
Q

What factors increase appetite?

A

opioids

growth hormone releasing hormones

65
Q

What is the effect of the opioid antagonist naltrexone?

A

Reduces the positive ‘hedonic valence’ of food

66
Q

What is the role of orexigenic neurotransmitters?

A

increase appetite

67
Q

What is the function of anorexigenic neurotransmitters?

A

decrease appetite

68
Q

Where are orexigenic and anorexigenic neurotransmitters found?

A

the hypothalamus

69
Q

What controls nutrient intake?

A

Signals from the periphery CNS controls nutrient intake

70
Q

What modulates responses to the CNS and Periphery?

A

Higher centres

71
Q

What environmental factors affect food intake

A
  • food preferences
  • emotions
  • lifestyle
  • environment
  • circadian rhythm
72
Q

Which receptors detect blood glucose?

A

[glucose]blood stimulates glucoreceptors in the hypothalamus

73
Q

What is the effect of increased Blood glucose?

A

Upregulation of satiety

74
Q

What is the effect of decreased blood glucose?

A

upregulation of hunger

75
Q

Why do diabetics feel hungry despite high blood glucose?

A

Diabetic patients feel hungry due to the lack of insulin present to decrease feeding behaviour
Individuals with insulin dependent diabetes melilitus (IDDM) are hyperphagic

76
Q

Explain IDDM patients are very rarely obese?

A

Aren’t obese because insulin is required for adipocytes to store fat
Excess calories consumed are wasted via inefficient utilisation via urine excretion

77
Q

What is calcitonin?

A

A hormone produced by the thyroid gland, involved in appetite reduction

78
Q

How does temperature affect appetite?

A

Cold environments stimulate feeding

Hot environments inhibit appetite

79
Q

How does the stomach regulate appetite?

A

Distension of a full stomach inhibits appetite
Contraction of an empty stomach stimulates appetite
Deposition of fat may control appetite via leptin

80
Q

Explain the effect of hormones on inhibiting food intake

A

CCK and somatostatin inhibit further food intake via vagus nerve

81
Q

Which pancreatic hormone helps regulate food intake and how?

A

Insulin is secreted into blood from the pancreas in direct proportion to the amount of fat stored in white adipose tissue

82
Q

How is insulin transported to the brain?

A

As insulin circulates through brain capillaries, a small amount of insulin is transported into the brain where it acts on insulin receptors on neurons with either:

  • net catabolic activity
  • net anabolic activity
83
Q

How do neurons and insulin receptors influence energy homeostasis?

A

These neurons influence

  • energy expenditure
  • food intake
  • amount of fat stored in body

by exerting a net catabolic action

84
Q

What effect does insulin have in adipocytes?

A

Insulin inhibits lipolysis in adipocytes

85
Q

What induces lipolysis?

A 
Gherlin 
Noradrenaline 
Adrenaline 
Growth Hormone 
Testosterone 
Cortisol
86
Q

Which hormones secreted by the endocrine pancreas regulate energy homeostasis?

A

Insulin, glucagon, amylin

- these are anorexigenic agents

87
Q

What is the function of insulin?

A

Reduces energy intake and suppresses hepatic glucose production by acting on the liver and forebrain

88
Q

What is the effect of glucagon?

A

Acts mainly at liver where it increases glucose production while generating a signal to reduce energy intake
-> relayed to hindbrain

89
Q

Where does amylin produce its effect?

A

Amylin acts directly on the hindbrain to reduce energy intake
NTS and Area Prostrema (AP) indicate stimulation

90
Q

What is the area Prostrema?

A

medularly structure controlling vomiting and ANS functions in the CNS

91
Q

What is the effect of leptin?

A

Administration can decrease food intake, induce weight loss and increase energy expenditure by increasing the expression of anorexigenic factors e.g.
POMC, CART, cocaine and CRH

92
Q

How does adipose tissue size affect leptin secretion?

A

Increased adipose tissue size = increased leptin secretion

93
Q

Explain how insulin and leptin work together

A

Insulin and leptin act agonistically in reducing food intake via action on receptors in brain

94
Q

What is the effect of increased leptin/insulin?

A

increased anorexigenic factors

  • increased energy expenditure
  • increased thermogenesis
  • diminished food intake
95
Q

What is the effect of decreased leptin/insulin?

A

increased orexigenic pathways

  • low metabolic rate
  • enhanced appetite
96
Q

How are leptin effects inhibited?

A

Binge eating (obesity) and Hyperaphia

97
Q

Explain the relationship of leptin and body fat

A

High correlation of leptin levels with body fat in humans

Hyperaphia and severe obesity occur with leptin deficiency or leptin receptor defects

98
Q

Outline the features of ghrelin

A
  • fast acting
  • stimulates food intake; orexigenic agent
  • released by stomach, pancreas, adrenals in response to
    nutritional status
  • circulating ghrelin levels increased, preprandial and
    decreased after a meal
99
Q

How does ghrelin induce food intake?

A

Increases central orexins (NPY and AgRP) to generate hunger signals
Suppresses leptin’s ability to stimulate anorexigenic factors

100
Q

What inhibits ghrelin secretion?

A

leptin

101
Q

What are the effects of obestatin?

A

suppresses food intake

antagonises ghrelin induced food intake

102
Q

How does obestatin mediate its effects?

A

Via different receptors to ghrelin
- encoded by ghrelin gene but opposing effects
produced

103
Q

Where is obestatin produced?

A

By stomach epithelial cells

Gastrointestinal (18 decks)

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