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BRS GASTROENTEROLOGY > 1b// Appetite > Flashcards

1b// Appetite Flashcards

1
Q

What was being overweight associated with before?

A

high-income countries, now also prevalent in low and middle income countries

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2
Q

What are the 3 main triggers of thirst?

A

body fluid osmolarity

blood volume is reduced

blood pressure is reduced

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3
Q

Which is the most potent stimulus for the trigger of thirst?

A

Plasma osmolarity increase is the more potent stimulus- change of 2-3% induces desire to drink

Decrease of 10-15% in blood volume or arterial pressure is required to produce the same response

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4
Q

Where is ADH stores?

A

anti diuretic hormone is stored in posterior pituitary

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5
Q

What is the other name for ADH?

A

vasopressin

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6
Q

What does ADH act on?

A

on kidneys to regulate the volume and osmolarity of urine
- collecting duct=> aquaporin 2 channel

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7
Q

What happens when plasma ADH is low/ high?

A

low= lots of urine (aka water diuresis)

high= little pee (anti diuresis)

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8
Q

How and where does the body measure osmolality?

A

osmoreceptors

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9
Q

osmolarity vs osmolality?

A

Osmolarity is the number of osmoles of solute per liter solution, which is different than osmolality, which is the osmoles of solute per kilogram of solution

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10
Q

What secretes ADH, and what is special about them?

A

neurones in hypothalamus
- Antidiuretic hormone is made by the hypothalamus and is secreted into the blood by the pituitary gland.

these neurones express osmoreceptors that are exquisitely sensitive to blood osmolarity (respond to very small change)

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11
Q

Where are osmoreceptors located?

A

in the hypothalamus

in the organum vasculosum of the lamina terminalis

in the subfornical organ

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12
Q

What are osmoreceptors?

A

sensory receptors for osmoregulation

found in the hypothalamus

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13
Q

How are osmoreceptors triggered to release ADH?

A

cells shrink when plasma more concentrated=>

proportion of cation channels increases- membrane depolarises=>

send signals to the ADH producing cells to increase ADH=>

Fluid retention invokes drinking

(and vice versa)

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14
Q

How is ADH release regulated in these neurones?

A
  • Under resting conditions, only a small proportion of the cation channels are active
  • Hypertonic stimulation leads to cell shrinking and increases the proportion of active cation channels
  • the resulting increase in positive charge influx depolarizes the membrane and increases neuronal action potential firing frequency
  • under hypotonic conditions, the channels are inhibited and the loss of cation influx causes hyperpolarization and inhibits firing
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15
Q

How is thirst decreased?

A

decreased by drinking even before sufficient water has been absorbed by the GI tract to correct plasma osmolarity

receptors in mouth, pharynx, oesophagus are involved

relief of thirst sensation via these receptors are short lived

thirst is only completely satisfied once plasma osmolality has decreased or blood volume or arterial pressure corrected

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16
Q

What is thirst?

A

sensation that is best described as the desire to drink

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17
Q

Why is the reason for drinking not always a physiological need?

A

sometimes prompted by habit, ritual cravings (for alcohol, caffeine or other drugs)

and even a desire to consume a fluid that will give a warming or cooling sensation

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18
Q

Where is there a delay in absorption of water?

A

delay in absorption of water in the GI tract and correction of plasma osmolality

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19
Q

Why is it important that there are mechanisms in place to avoid excessive fluid intake?

A

important as although the kidney can deal with fluid overload=> there is a wastage of energy and interference of nutrient absorption (sodium drive)

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20
Q

What system controls blood pressure/ volume?

A

the renin-angiotensin-aldosterone system

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21
Q

Describe the enin-angiotensin-aldosterone system.

A

Renin is an aspartic protease protein & enzyme secreted by the kidneys…
- Renin activates the renin-angiotensin system by cleaving angiotensinogen, produced by the liver to yield angiotensin.
- When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin into renin and secrete it directly into the circulation.

Angiotensinogen is a precursor protein produced in the liver and cleaved by renin to form angiotensin I.
Angiotensin-converting enzyme (ACE) produced in the lung, etc. cleaves two amino acids from angiotensin I to produce angiotensin ll approx. 30-60 minutes after the drop in blood pressure

Angiotensin Il is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them and causing the release of aldosterone.

Aldosterone is a mineralocorticoid released from the zona glomerulosa in the adrenal cortex.
Aldosterone has a major role in sodium conservation.
- It influences the reabsorption of sodium and excretion of potassium indirectly influencing water retention.

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22
Q

How is body mass regulated?

A

physiologically

humans regulate body mass in a way that changes in adipose tissue activate responses that favour the return to their previous weight

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23
Q

Describe body weight homeostasis.

A

Weight was stable for a long time despite no conscious effort to balance intake and expenditure

Most individual adults maintain a relatively stable weight over long periods

A reduction in fat mass increases food intake and reduces energy expenditure

Adipose tissue expansion reduces food intake and increases energy expenditure

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24
Q

What happens during weight augmented overfed state?

A

Increased sympathetic NS activity

Increased E expenditure

Decreased food intake/ hunger

Weight loss

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25
Q

What happens during weight reduced underfed state?

A

decreased sympathetic NS activity

Decreased E expenditure

Increased hunger/ food intake

Decreased thyroid function

Increased weight gain

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26
Q

Are there studies for the body’s mechanisms against weight gain/ loss?

A

yes for anti body reduction

yet to be discovered for anti weight gain

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27
Q

What part of the brain is critical in the regulation of food intake?

A

the hypothalamus is critical in the regulation of food intake
- contains neural circuits which produce a number of peptides that influence food intake

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28
Q

Describe appetite regulation.

A
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29
Q

What are appetite supressants called?

A

anorectic

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30
Q

What are appetite stimulants called?

A

orexigenic

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31
Q

What is the arcuate nucleus?

A

arcuate nucleus of the hypothalamus is an aggregation of neurons in the mediobasal hypothalamus adjacent to 3rd ventricle

brain area involved in the regulation of food intake

the most important site in the hypothalamic integration of energy balance

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32
Q

What does the arcuate nucleus do?

A

produces both appetite increasing (orexigenic) and appetite suppressant (anorectic) peptides

  • one of the terminal fields of these orexigenic and anorexigenic neurones is the paraventricular nucleus
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33
Q

What is the PVN?

A

paraventricular nucleus of the hypothalamus lays adjacent to the 3rd ventricle

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34
Q

What is in the PVN?

A

contains neurones that project to the posterior pituitary

these projecting neurones secrete oxytocin and vasopressin affecting osmoregulation, appetite and stress reaction of the body

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35
Q

What does the lateral hypothalamus produce?

A

orexigenic peptides

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36
Q

What is the VMH and what is it associated with?

A

ventromedial hypothalamus which is associated with satiety

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37
Q

What do lesions of the VMH lead to?

A

obesity

there is a debate to what extent this is true

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38
Q

What in the VMH is suggested to regulate feeding behaviour?

A

melanocortins in the VMH

e.g., food intake decreases when arcuate nucleus pro-opiomelanocortin (POMC) neurons activate VMH brain-derived neurotrophic factor neurons

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39
Q

What structural adaptation of arcuate nucleus benefits it and why?

A

incomplete blood brain barrier, allows access to peripheral hormones

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40
Q

What feeding signals does the arcuate nucleus consider?

A

peripheral and central

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41
Q

What are the neuronal populations in the arcuate nucleus?

A

Stimulatory (NPY/ AGRP neuron)

Inhibitory (POMC neuron)

42
Q

What are the stimultory NPY and AGRP neurons?

A

neuropeptide y= NPY
agouti-related peptide= AGRP

made by the NPY and AGRP neurons

43
Q

What is the most important neuron of the inhibitory pathway?

A

pro-opiomelanocortin (POMC) neuron

44
Q

Where is stimulating NPY and AGRP neuron found?

A

only in the hypothalamic arcuate nucleus

45
Q

How do NPY and AGRP work?

A

NPY=> stimulating food intake by increasing neuropeptide Y signalling

AGRP=> reducing melanocortin signalling via the release of agouti-related peptide, an endogenous melanocortin receptor antagonist

46
Q

What do the NPY and AGRP neurons also express and how are they activated? Furthermore what conditions cause certain food behaviours due to this mechanism?

A

also express receptors for leptin and insulin–> they’re activated by a decrease of leptin or insulin signalling

fasting, uncontrolled diabetes and genetic leptin deficiency
- food intake increases via this mechanism

47
Q

What else are neurons in ARC responsible for?

A

integrating info and providing inputs to other nuclei in the hypothalamus

48
Q

What is the most important nuclei in ARC?

A

the PVN (paraventricular nucleus)

49
Q

What does POMC do to feeding?

A

decreases

50
Q

What does NPY do to feeding?

A

increases

51
Q

What does the function of the arcuate nucleus rely on?

A

on its diversity of neurons and its central role in homeostasis

52
Q

What else, other than feeding, is the arcuate nucleus involved in?

A

fertility and CVD regulation

53
Q

How does the melanocortin system work?

A

decreases food intake

alpha-MSH=> melanocyte stimulating hormone

54
Q

What is the central melanocortin system?

A

a collection of the previously discussed CNS circuits such as:
- neuropeptide Y and agouti gene-related protein
- pro-opiomelanocortin

55
Q

What are melanocortins?

A

products of the POMC gene
- a classic example is a-MSH

56
Q

Why is the central melanocortin system important?

A

central regulator of E balance, involved in both feeding behaviour and E expenditure

57
Q

How does a-MSH lead to decreased weight?

A

melanocortin-4 receptors (MC4R) expressed in PVN
- a-MSH stimulates MC4R and leads to reduction of appetite and weight
- ARGP inhibits

58
Q

What are human CNS mutations affecting appetite?

A

No NPY or Agrp mutations associated with appetite in humans.

POMC deficiency and MC4-R mutations cause morbid obesity.

*Mutations not responsible for the prevalence of obesity - but useful to explain signalling.

59
Q

What are signals for feeding from other brain regions? (3)

A

Higher centres
- Amygdala - emotion, memory.

Other parts of the hypothalamus, e.g. lateral hypothalamus

Vagus to brain stem to hypothalamus.

60
Q

How does the amygdala play a role in appetite?

A

important role in controlling reward-related motivation pathways affecting appetite

61
Q

What does the lateral hypothalamus do related to appetite?

A

produced appetite stimulant peptides

62
Q

What is the ventromedial hypothalamus associated to in appetite?

A

ventromedial hypothalamus is associated with satiety

63
Q

How is neuronal information from the digestive tract carried?

A

to the brainstem via the vagus nerve

64
Q

What is brainstem linked to, and what is that linked to?

A

linked to the hypothalamus, which is linked to amygdala

65
Q

What is the adipostat mechanism and what does it consist of?

A

keeps an individual’s fat mass within range despite changes in diet and activity

consists of 2 neuronal pathways in the hypothalamus

66
Q

How does the adipostat mechanism work?

A

Circulating hormone produced by fat

Hypothalamus senses the concentration of hormone.

Hypothalamus then alters neuropeptides to increase or decrease food intake

67
Q

Does the story of this mouse make sense?

A

leptin is missing in the ob/ ob mouse

68
Q

What makes leptin?

A

Made by adipocytes in white adipose tissue & enterocytes in the small intestine

69
Q

Where does leptin circulate?

A

in plasma

70
Q

Where does leptin act?

A

Acts on the hypothalamus regulating appetite (intake) and thermogenesis (expenditure).

act on cell receptors in the arcuate and ventromedial nuclei in the hypothalamus
- consequently mediating feeding and thermogenesis

71
Q

When is leptin high/ low?

A

low when low body fat

high when high body fat

72
Q

What does leptin do (basic)?

A

hormone that decreases food intake, and increases thermogenesis

it helps with energy balance by inhibiting hunger

73
Q

What is the primary function of leptin? And what are extra roles of leptin?

A

regulation of adipose tissue mass

  • also plays a role in the development of atherosclerosis through the innate immune system
  • low levels discovered in alzheimer’s disease and depression
  • also facilitates surfactant production in the foetus
74
Q

What is congenital leptin deficiency?

A

a condition that causes severe obesity

in these children leptin has been effective in reducing body weight

only few people known to have this defect

subjects carrying the mutations are of normal weight at birth, but they are constantly hungry and quickly gain weight

they had high body fat, but low serum leptin

75
Q

When does leptin increase?

A

as body fat increases

76
Q

What does leptin correlate with? And what does this mean?

A

serum leptin concs correlated with the % body fat
-> suggesting that most obese people are insensitive to endogenous leptin production
-> their leptin is high (in obese people)

77
Q

What are the 3 mechanisms of leptin issues?

A
  1. insufficient production (aka low leptin)
  2. defective leptin receptor signalling- reduced/ normal leptin level despite high adipose tissue mass
  3. decreased sensitivity to leptin, resulting in an inability to detect satiety despite high energy stores and high levels
78
Q

What is the mechanism of leptin?

A
79
Q

Describe leptin resistance.

A

Leptin circulates in plasma in concentrations proportional to fat mass

Overweight humans have ↑leptin

Obesity due to leptin resistance - hormone is present but
doesn’t signal effectively

Leptin is ineffective as a weight control drug.

80
Q

Why do we feel less hungry after a meal?

A

Hormonal signals from the gut

bulk in stomach- limited so not really
nutrients in circulation- limited so not really

81
Q

What are the GI hormones?

A

aka gut hormones

a group of hormones secreted by enteroendocrine cells in the stomach, pancreas, and small intestine

control various functions of digestive organs such as motility and appetite regulation

82
Q

What are the 2 main gut hormones?

A

Ghrelin and Peptide YY

they regulate appetite

83
Q

What does Ghrelin do?

A

stimulates appetite, increases gastric emptying

84
Q

What does Peptide YY do?

A

inhibits food intake

85
Q

When are serum levels of ghrelin highest?

A

before melas
- helps prepare for food intake by increasing gastric motility and acid secretion

86
Q

How is ghrelin linked to the hypothalamus?

A

Directly modulates neurons in the arcuate nucleus
* Stimulates NPY/Agrp neurons.
* Inhibits POMC neurons.

87
Q

Does ghrelin decrease or increase appetite?

A

increase

88
Q

What is ghrelin involved with?

A

regulation of reward, taste sensation, memory and circadian rhythm

89
Q

What hormone does this graph relate to and how can you tell?

A

Ghrelin, highest before meals, and decreases after meals

between meals there is a diurnal rhythm, and slowly increases during the day

90
Q

How is ghrelin measured?

A

radioimmunoassay in plasma samples

91
Q

What happens to humans who get iv ghrelin?

A

there was a clear cut increase in E consumption by every individual from a free-choice buffet during ghrelin compared with saline infusion

92
Q

What is PYY and what does it do? And how is it secreted? and what does it stimulate and inhibit?

A

Peptide tyrosine tyrosine

Short peptide released in the terminal ileum (TI) and colon in response to

Reduces appetite – can be digested or injected IV

Food arriving to the TI and colon results in PYY release

Stimulates POMC neurons

Inhibits NPY release

93
Q

How many AA long is PYY?

A

36

94
Q

What encodes peptide tyrosine tyrosine?

A

PYY gene

95
Q

Is PYY anorexigenic or orexigenic?

A

anorexigenic

96
Q

What foods increase release of PYY?

A

dietary fibres, whole grains, consumed and enzymatic breakdown of crude fish proteins

97
Q

What do dietary fibres, whole grains, consumed and enzymatic breakdown of crude fish proteins do to satiety?

A

induce satiety
via stimulation of POMC and inhibition of NPY release

98
Q

What is amount of PYY released from the GI tract proportional to?

A

calorie content of a meal

99
Q

What is the effect of PYY on food intake and hunger in humans?

A
100
Q

What co-morbidities is obesity associated with? (10)

A

depression
stroke
sleep apnoea
bowel cancer
osteoarthritis
gout
peripheral vascular disease
diabetes
hypertension
myocardial infarction

101
Q

What does thi figure demonstrate?

A
102
Q

Does this summary make sense?

A

Y/ N

BRS GASTROENTEROLOGY (25 decks)

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