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Control of food intake Flashcards

1
Q

What enables storage of food in the stomach?

A

Autonomic system enables the storage of food in the stomach

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2
Q

What part expands during accommodation?

A

Fundic part expands when accommodating

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3
Q

What are the control factors of accommodation?

A

VIP and NO are accommodation control factors

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4
Q

What hormone is important in emptying and why?

A

Ghrelin because it is Important in initiating the feeling of hunger

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5
Q

What is NO?

A

A relaxation factor

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6
Q

What is the relaxation of fundus mediated by and how many types can it be differentiated into?

A

Mediated by reflexes and can be differentiated into 3 types

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7
Q

Name the 3 types of reflexes involved in the relaxation of the fundus and one component mediator

A 
o	Receptive (mechanical stimulation of pharynx – mechanoreceptors, sight) 
o	Adaptive (vagal innervation (NO/VIP), tension of stomach) 
o	Feedback (nutrients, CCK)
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8
Q

What are the receptive, adaptive and feedback-relaxation mediated by

A

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.

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9
Q

What is PACAP isolated from and what is it shown to stimulate?

A

o Isolated from pituitary and shown to stimulate adenylate cyclase activity in the anterior pituitary

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10
Q

Levels of PACAP in the body

A

High levels in the brain but also found in the gut

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11
Q

What does PACAP mediate?

A

o Mediates neuronal regulation of gastric acid secretion; intestinal motility

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12
Q

What does PACAP stimulate?

A

o Stimulates relaxation of colonic smooth muscle and stimulates pancreatic secretions; stimulates insulin and glucagon secretion in humans.

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13
Q

What does vagotomy impair?

A

Impairs accommodation and emptying

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14
Q

What is vagotomy a cause for in some patients?

A
  • A cause for early satiety in some patients
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15
Q

What does vagotomy reduce?

A
  • Vagotomy reduces accommodation and gastric compliance
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16
Q

What can prior gastric surgery to vagotomy result in?

A
  • Prior gastric surgery may result in gastroparesis
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17
Q

What is gastric compliance?

A

Accommodation and perception of distention

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18
Q

Define hunger

A

-Discomfort caused by a lack of food and the desire to eat

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19
Q

Define appetite

A

-Desire to satisfy the body’s need of food

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20
Q

Define aphagia

A

-Inability or refusal to swallow

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21
Q

Define hyperphagia

A

An abnormal desire for food

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22
Q

What type of control is food intake?

A

Hypothalamic control

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23
Q

What are the reasons for difference in BMI?

A
  • Genes(70%)

- How much we eat and its composition

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24
Q

What, in the hypothalamus, regulates feeding?

A
  • The balance of stimulating and inhibiting forces in the hypothalamus regulates feeding
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25
Q

How does the hypothalamus control hunger?

A

Base of the hypothalamus has several nuclei that regulate energy homeostasis

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26
Q

What neurotransmitters have been found in the hypothalamus?

A
  • Orexigenic and Anorexigenic neurotransmitters have been found in the hypothalamus
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27
Q

What do orexigenic neurotransmitters do?

A

Increase appetite

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28
Q

What do anorexigenic neurotransmitters do?

A

Decrease appetite

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29
Q

What is feeding behavior/food intake modulated b?

A

Modulated by hypothalamic sites

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30
Q

What is the lateral hypothalamus(LH) the site of?

A

-Hunger centre

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31
Q

What is the ventromedial nucleus(VMN) the site of?

A

-Satiety centre

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32
Q

What does VMN have the ability to restrain and what does this lead to?

A

– Have the ability to restrain feeding if required; lesion →↑ appetite, with weight gain that tends to persist

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33
Q

What does DMN modulate?

A

Modulates energy intake(hunger center)

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34
Q

What is released into DMN and what does this increase?

A

– Release NPY into DMN and increase feeding

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35
Q

What does PVN modulate?

A

Modulates feeding behaviour

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36
Q

What does PVN control?

A

Control feeding behaviour

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37
Q

What do NPY, opiods, GABA increase?

A

Increase feeding

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38
Q

What does leptin do to food intake?

A

Decreases food intake

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39
Q

In the arcuate nucleus, what do the neurons produce?

A

Neurons produce orexigenic signals(NPY, the opioids, dynorphin, β-endorphin, POMC, galanin, amino acids, and glutamate)

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40
Q

What is the SCN responsible for?

A

responsible for controlling circadian rhythms

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41
Q

Where is the SCN located?

A

In the hypothalamus

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42
Q

What is the SCN directly above?

A

directly above the optic chiasm

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43
Q

What is the medial amygdaloid nucleus a sub-region of?

A

Sub-region of the amygdaloid complex

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44
Q

What does a medial amygdaloid nucleus participate in?

A

Participates in the regulation of food intake

– 5-HT (via 5-HT2C and 5-HT1A): regulates appetite and food intake

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45
Q

How is appetite regulated?

A

Appetite is regulated by the balance between an appetite stimulating pathway that releases agouti-related peptide (AgRP) and neuropeptide Y (NPY), and an appetite suppressing pathway that releases alpha-melanocyte stimulating hormone (alpha-MSH)

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46
Q

Steps involved in appetite stimulating pathway

A

o The appetite suppressing neurons make the precursor pro-opiomelanocortin (POMC), which is broken down into alpha-MSH, which in turn binds to melanocortin 4 receptors (MC4R) to suppress appetite. Shown here is no occupancy of MCR4 receptors by alpha-MSH, and thus stimulation of appetite.

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47
Q

Steps involved in appetite repressing pathway

A

A serotonin 5HT2C agonist, such as meta-chlorphenylpiperazine (mCPP), hypothetically binds to 5HT2C receptors on POMC neurons in the appetite suppressing pathway, activating POMC neurons and leading to release of alpha-melanocyte stimulating hormone (alpha-MSH), which binds to melanocortin 4 receptors (MC4R) to suppress appetite.

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48
Q

What does zimelidine do?

A

inhibits the reuptake of 5-HT from synaptic cleft, so 5HT persists and able to mediate its effects in suppressing appetite

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49
Q

What are the side effects of zimelidine?

A

Side effects are dry mouth, increased sweating (hyperhidrosis), vertigo, nausea,

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50
Q

What is the role of the prefrontal cortex?

A

Integration of sensory information from inside and outside the body

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51
Q

What dose the prefrontal cortex receive and from where?

A

– Receive emotional and cognitive information from the limbic system

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52
Q

What is the limbic system?

A

complex system of nerves and networks in the brain; areas concerned with instinct and mood. May control emotions, pleasure (fear, anger, etc.)

53
Q

What is the MeA and what has it been described as?

A
  • The medial amygdaloid nucleus (MeA) is a sub-region of the amygdaloid complex that has been described as participating in regulating food intake
54
Q

What is serotonin known to play as?

A

o Serotonin (5-HT) has been known to play an important role in regulating appetite and food intake.

55
Q

What is the cortico-limbic mechanism of reward under control of?

A

Under executive control of the prefrontal cortex

56
Q

What is the control of food intake an integration of?

A

Integration of many signals

57
Q

What does DMN modulate?

A

Modulates energy intake

58
Q

What does the destruction of DMN lead to?

A

Destruction leads to hyperphagia & obesity

59
Q

What does the DMN also recieve and also has what type of cells?

A

 DMN also receive projections from agRP/NPY neurons from ARC; it also has NPY-expressing cells

60
Q

What is the PFA?

A

 A very sensitive hypothalamic site for NPY-induced eating

61
Q

How is NPY found?

A

NPY is found in high concentrations within neurons of hypothalamus

62
Q

What happens of NPY is injected into the hypothalamus?

A

if injected into the hypothalamus, it stimulates powerful stimulus to eat

63
Q

What is the FX and what does it carry?

A

 C-shaped bundle of nerve fibres in the brain that carries signals from the hippocampus to the mammillary bodies and then to the anterior nuclei of thalamus

64
Q

What system is FX part of and what is it involved in?

A

 It is part of the limbic system – involved in memory and recall

65
Q

What is the LHA?

A

Hunger center

66
Q

What is the VMN?

A

Satiety center

67
Q

What is the ME part of and what is it integral to?

A
  • Part of hypothalamus

- Integral to the hypophyseal portal system

68
Q

What does the stimulation of ventromdial wall of paraventricular nucleus lead to?

A

Leads to aphagia

69
Q

What do lesions of ventromedial wall of paraventricular nucleus lead to?

A

Lead to hyperphagia

70
Q

What does the brain contain?

A

Has glucostats

71
Q

What is the lateral hypothalamus the center of?

A

Feeding center

72
Q

What does lesions of the lateral hypothalamus lead to?

A

Aphagia

73
Q

What do opioids and growth hormones do to appetite?

A

Increase appetite

74
Q

What is Naltrexone?

A

An opioid antagonist

75
Q

What does Naltrexone reduce?

A

Reduces the positive hedonic valence of food

76
Q

What does removal of lateral hypothalamus cause and lead to?

A

Causes hypophagia, leading to death due to severe weight loss

77
Q

What dose the removal of the ventromedial hypothalamus cause and lead to?

A

Causes hyperphagia, leading to weight gain and severe obesity

78
Q

What signals control nutrient intake?

A

Signals from periphery and CNS control nutrient intake

79
Q

What factors affect if food is sought or not?

A
  • Food preferences
  • Emotions
  • Environment
  • Life style
  • Circadian rhythm – limits food intake to certain times (in some people)
80
Q

What does blood glucose concentration stimulate?

A

Stimulates gluco-receptors in hypothalamus

81
Q

What does a decrease in blood glucose concentration lead to?

A

Leads to up-regulation of hunger

82
Q

What does an increase in blood glucose concentration lead to?

A

Leads to up-regulation of satiety

83
Q

Why do diabetic patients feel hungry despite an increase in blood glucose concentration?

A

• Cold environments stimulate feeding while hot environments inhibit appetite

84
Q

What does distension of a full stomach inhibit?

A

Inhibits appetite

85
Q

What does the contraction of an empty stomach stimulate?

A

Stimulates appetite

86
Q

What does insulin decrease?

A

Insulin decreases feeding behavior

87
Q

What are people that are suffering with IDDM?

A

They are hyperphagic and such individuals are not obese because insulin is required for adipocytes to store fat

88
Q

What does calcitonin reduce?

A

Reduces appetite.

89
Q

What does insulin inhibit?

A

Inhibits lipolysis in adipocytes

90
Q

What induces lipolysis?

A
  • Ghrelin, NA, adrenaline, growth hormone, testosterone and cortisol induce lipolysis
91
Q

What are insulin, glucagon and amylin secreted from and what do they participate in?

A
  • Insulin, glucagon and amylin are all secreted from the endocrine pancreas, and all participate in the regulation of energy homeostasis
92
Q

Where does insulin act at and what does it do ?

A

o Insulin acts at both the liver and the forebrain to reduce energy intake as well as to suppress hepatic glucose production.

93
Q

Where does glucagon mainly act at and what does it do?

A

o Glucagon acts mainly at the liver where it increases glucose production while generating a signal to reduce energy intake that is relayed to the hindbrain.

94
Q

Where does amylin directly act and to do what?

A

o Amylin acts directly at the hindbrain to reduce energy intake

95
Q

What does fat ingestion cause the release of?

A

• Fat ingestion causes CCK release and the slowing of gastric emptying (sense of fullness)

96
Q

What does CCK and somatostatin inhibit?

A

inhibit further food intake; satiety factors

97
Q

What does an injection of CKK in the brain reduce?

A

Reduction of appetite

98
Q

What do leptin and ghrelin act on?

A

• Leptin and ghrelin act reciprocally on food intake

99
Q

What does the stimulation of their receptors in hypothalamus change?

A

Changes in food intake

100
Q

Where is leptin found?

A

Found in white adipose tissue

101
Q

What does leptin control?

A

Controls fat stores by operating a feedback mechanism between adipose tissue and brain

102
Q

What happens as adipose tissue size increases?

A

Increase in leptin secretion

103
Q

How do insulin and leptin act and via what?

A
  • Insulin and leptin act agonistically in reducing food intake via action on receptors within the brain
104
Q

What does satietin suppress and without causing what?

A
  • Satietin suppresses food intake and weight without causing conditioned taste aversion
105
Q

What pathway prevails when there’s an abundance of leptin or insulin?

A
  • The anorexigemic pathway prevails:
    - Increase of energy expenditure
    - Increase of thermogenesis
    - Diminished food intake
106
Q

What does decreasd petin and insulin serum concentrations lead to?

A

Lead to activation of orexigenic pathways:

  • Low metabolic rate
  • Enhanced appetite
107
Q

Where is the leptin gene mainly expressed?

A

Expressed mainly in adipocytes

108
Q

What can administration decrease, induce and increase?

A

• Administration can decrease food intake, induce weight loss and increase energy expenditure

109
Q

Who does hyperphagia and severe obesity occur in?

A

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

110
Q

What does leptin increase the expression of?

A

• Increases the expression of anorexigenic factors (pro-opiomelanocortin (POMC), cocaine-and amphetamine-regulated transcript (CART), corticotrophin-releasing hormone (CRH), neurotensin)

111
Q

What does leptin stimulate?

A

Stimulates metabolic rate

112
Q

What does leptin inhibit, which goes on to stimulate what?

A

• Inhibits neuropeptide Y, which stimulates feeding

113
Q

Can one be resistant to the effects of leptin?

A

• Yes; → binge eating, despite adequate or growing adipose tissue (obese)

114
Q

What is ghrelin?

A

An appetite inducing hormone

115
Q

How does Ghrelin act and what does it stimulate?

A

Fast-acting and stimulates food intake

116
Q

What is ghrelin released by?

A
  • Released by stomach, pancreas, adrenals in response to nutritional status
117
Q

When do ghrelin levels increase and decrease?

A

Increase preprandially and decrease after a meal

118
Q

What does ghrelin increase?

A
  • Increases central orexins
119
Q

How can ghrelins secretion be inhibited?

A
  • Its secretion can be inhibited by leptin
120
Q

What is ghrelin produced by and where in the stomach?

A
  • In the stomach, ghrelin is produced by cells called P/D1 cells in the upper section of the stomach
121
Q

What inhibits the expression of ghrelin ?

A

Increased levels of glucose inhibits its expression in the P/D1 cells

122
Q

What is Obestatin produced by?

A

Produced by epithelial cells of the stomach

123
Q

What is Obestatin encoded by?

A

• Encoded by ghrelin gene

124
Q

What does Obestatin oppose?

A

Opposes effect of ghrelin on food intake

125
Q

What does Obestatin suppress?

A

Supresses food intake

126
Q

What does Obeostatin antagonize?

A

• Antagonises ghrelin-induced food intake (and growth hormone secretion)

127
Q

An imbalance of what has a role in obesity?

A

• Imbalance of ghrelin and obestatin has a role in obesity

128
Q

What does Obestatin mediate its effect via?

A

Obestatin mediates its effects via different receptors to ghrelin

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