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Year 2 - BRS > 6.2 - Appetite > Flashcards

6.2 - Appetite Flashcards

1
Q

What are the three main triggers through which the body controls thirst?

A
  • body fluid osmolality increase
  • blood volume is reduced
  • blood pressure is reduced
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2
Q

Which of the three triggers is the most potent stimulus for thirst?

A
  • plasma osmolality increase - change of 2-3% induces strong desire to drink
  • decrease of 10-15% in blood volume or arterial pressure is required to produce the same effect
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3
Q

What molecule is used by the body to regulate osmolality?

A

Anti-diuretic hormone (ADH) AKA vasopressin

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4
Q

How does ADH regulate osmolality?

A
  • acts on kidneys in the collecting duct through the aquaporin 2 channel to regulate volume and osmolality of urine
  • when plasma ADH is low, a large volume of urine is excreted (water diuresis)
  • when plasma ADH is high, a small volume of urine is excreted (anti-diuresis)
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5
Q

Where is ADH stored?

A

In the posterior pituitary

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6
Q

How does the body detect changes in osmolality?

A
  • through osmoreceptors - sensory receptors
  • ADH secreted in neurons in hypothalamus, these neurones express osmoreceptors that are sensitive to blood osmolality
  • changes in osmolality leads to secretion or reduction of ADH
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7
Q

Where are osmoreceptors found?

A

Hypothalamus

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8
Q

Which two regions are osmoreceptors found within the hypothalamus?

A
  • organum vasculosum of the lamina terminalis (OVLT)
  • subfornical organ (SFO)
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9
Q

How do osmoreceptors respond when the plasma is hypertonic?

A
  1. under resting conditions, a set proportion of cation channels in osmoreceptors are active
  2. hypertonic stimulation leads to cell shrinking (as fluid moves out) and increases the proportion of active cation channels
  3. results in increasing positive charge influx which depolarises membrane
  4. this increases neuronal action potential firing frequency, increasing ADH production
  5. leads to fluid retention and invokes thirst/drinking
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10
Q

How do osmoreceptors respond when the plasma is hypotonic?

A
  • same as hypertonic but vice versa:
  • cation channels are inhibited
  • loss of cation influx causes hyperpolarisation and inhibits neuronal firing
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11
Q

Define thirst?

A

The desire to drink

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12
Q

What can cause thirst?

A
  • not always a physiological need
  • sometimes prompted by habit, ritual cravings (for alcohol, caffeine or drugs etc)
  • desire to consume fluid that will give a warming or cooling sensation
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13
Q

What is the issue with water absorption and plasma osmolality correction?

A
  • there is a delay between water absorption in GI tract and correction of plasma osmolality, as water is absorbed and circulates around body
  • so, overdrinking can be an issue - there are mechanisms in place to avoid excessive fluid intake
  • important as although kidney can deal with fluid overload by expelling more water, this wastes energy and interferes with nutrient absorption (sodium driven)
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14
Q

How does the body prevent excessive fluid intake?

A
  • thirst is decreased by drinking even before sufficient water has been absorbed by GI tract to correct plasma osmolality
  • receptors in mouth, pharynx and oesophagus are involved in relieving thirst
  • however, relief of thirst sensation via these receptors is short-lived
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15
Q

When is thirst completely satisfied?

A

Once plasma osmolality has decreased, or blood volume/arterial pressure are corrected

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16
Q

What is the renin-angiotensin-aldosterone system (RAAS) in relation to thirst?

A

The less effective way of controlling thirst

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17
Q

Describe the renin-angiotensin-aldosterone system (RAAS).

A
  • when BP/renal blood flow is reduced, juxtaglomerular apparatus/cells secretes renin
  • renin (AKA angiotensinogenase) is an enzyme that cleaves angiotensinogen secreted by the liver to activate it to become angiotensin I
  • angiotensin I –> angiotensin II (removal of two AAs) by ACE, which occurs in lungs
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18
Q

What are the effects of angiotensin II? (4)

A
  • induces thirst
  • binds to receptors on intraglomerular messenger cells, which causes cells to contract along with blood vessels around them –> leads to aldosterone release in zona glomerulosa of adrenal cortex
    • aldosterone retains water through Na+Cl- absorption and K+ secretion
  • causes ADH secretion
  • activates sympathetic NS causing vasoconstriction
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19
Q

What three types of drugs inhibit the RAAS system and are therefore used in treating hypertension?

A
  • direct renin inhibitors
  • ACE inhibitors
  • angiotensin II receptor blockers
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20
Q

Describe a brief history of body weight homeostasis research.

A
  • Neuman 1902 - his weight was stable for a long time despite no conscious effort to balance out intake and expenditure
  • Passmore 1971 - most individual adults maintain a relatively stable weight over long periods - his findings also suggested
    • 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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21
Q

What does the body do if fat mass is reduced (underfed state)?

A
  • decreased sympathetic nervous system activity
  • decreased energy expenditure
  • increased hunger/food intake
  • decreased thyroid activity
  • = weight regain
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22
Q

What does the body do if fat mass is increased (overfed state)?

A
  • increased sympathetic nervous system activity
  • increased energy expenditure
  • decreased hunger/food intake
  • weight loss
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23
Q

What body system defends against rapid expansion of fat mass?

A

Yet to be discovered

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24
Q

Discovery of what molecule helped us understand the system that is activated following reduction in fat mass?

A

Leptin

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25
Q

Where does appetite regulation occur?

A

Hypothalamus - increases or decreases energy expenditure and food intake

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26
Q

What peripheral stimuli are involved in appetite regulation?

A
  • ghrelin, PYY and other gut hormones - communicate through vagus nerve –> brainstem –> communicates with hypothalamus –> communicates with higher CNS regions like amygdala
  • neural input from the periphery and other brain regions
  • leptin (via leptin control system)
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27
Q

What does orexigenic and anorectic mean?

A
  • orexigenic - appetite stimulant
  • anorectic - appetite suppressive
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28
Q

What is the arcuate nucleus in the hypothalamus responsible for?

A
  • aggregation of neurones in the medial basal part of the hypothalamus
  • adjacent to third ventricle
  • produces both orexigenic (appetite increasing) and anorectic (appetite suppressive) peptides
  • project to paraventricular nucleus
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29
Q

When does the arcuate nucleus decrease food intake?

A

When its pro-opiomelanocortin (POMC) neurones activate

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30
Q

What is the paraventricular nucleus (PVN) in the hypothalamus responsible for?

A
  • lays adjacent to third ventricle
  • contains neurones that project to posterior pituitary and secrete oxytocin and ADH, to regulate osmoregulation, appetite and stress reaction of body
  • MC4R receptors expressed in PVN
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31
Q

What is the lateral nucleus in the hypothalamus responsible for?

A

Produces only orexigenic peptides

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32
Q

What is the ventromedial hypothalamus (VMH) responsible for?

A
  • associated with satiety
  • lesions in this region in rats leads to severe obesity
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33
Q

What other hypothalamic factors are implicated in appetite regulation? (3)

A
  • endocannabinoids
  • AMP (activated protein kinase)
  • protein tyrosine phosphatase
34
Q

What does the arcuate nucleus do?

A
  • brain area involved in regulation of food intake
    • (most important site in the hypothalamic integration of energy balance)
  • integrates peripheral and central feeding signals
35
Q

What is the BBB of the arcuate nucleus like and why?

A

Incomplete BBB to allow access to peripheral hormones

36
Q

What two neuronal populations does the arcuate nucleus have?

A
  • stimulatory (orexigenic) - NPY/AGRP neuron
  • inhibitory (anorectic) - POMC neuron
37
Q

What peptides do stimulatory NPY/AGRP neuron produce and what do these do?

A
  • neuropeptide Y (increased NPY signalling) - direct activation of orexigenic peptides in PVN
  • Agouti-related peptide (AGRP) - reduces melanocortin signalling as it is an endogenous melanocortin receptor antagonist
  • these stimulate food intake
38
Q

What other receptors does the arcuate nucleus contain? (2)

A

Receptors for leptin and insulin, activated by decrease/increase in leptin/insulin signalling

39
Q

What kinds of conditions lead to increased food intake through leptin/insulin receptors in arcuate nucleus? (3)

A
  • fasting
  • uncontrolled diabetes
  • general leptin deficiency
40
Q

What do circulating peripheral hormones in the blood do when they reach the hypothalamus?

A
  • cross incomplete BBB and penetrate arcuate nucleus
  • either NPY/AGRP neurones (increases feeding) or POMC neurones (decreases feeding) activated –> both go to paraventricular nucleus
41
Q

Besides feeding, what other functions is the arcuate nucleus involved in? (2)

A
  • fertility
  • cardiovascular regulation
42
Q

How does the melanocortin system work?

A
  • melanocortin 4 receptors (MC4R) are expressed on paraventricular nucleus
    • activation of MC4R leads to decrease in appetite & weight & food intake
  • AGRP neurones in arcuate nucleus release AGRP which act on MC4R as antagonists
  • POMC neurones produce melanocortins - classic example is alpha-MSH - which act on MC4R as agonists (decreased food intake)
43
Q

What do NPY or AGRP mutations do to appetite?

A

No NPY or AGRP mutations associated with appetite in humans

44
Q

What can POMC deficiency cause?

A

Morbid obesity

45
Q

What can MC4R mutations cause?

A

Morbid obesity

46
Q

What are looking into these human CNS mutations affecting appetite useful for?

A

Not to explain prevalence of obesity, but useful to explain signalling

47
Q

What signals from other brain regions (outside arcuate nucleus and PVN) are involved in controlling appetite? (3)

A
  • higher centres e.g. amygdala - responsible for emotion and memory, and controlling reward-related motivation pathways which has strong effect on appetite
  • other parts of hypothalamus - lateral hypothalamus and ventromedial hypothalamus
  • vagus communication from digestive tract to brainstem then hypothalamus then amygdala (these three centres work together to regulate appetite)
48
Q

What is the adipostat mechanism?

A

The body’s thermostat i.e. control of energy expenditure through thermoregulation which keeps individual’s fat mass within narrow range despite changes to diet or daily activity

49
Q

How does adipose tissue interact with hypothalamus for it to regulate food intake?

A
  • circulating hormones are produced by adipose tissue - the more adipose tissue, the more hormones being produced
  • hypothalamus senses concentration of hormones then alters neuropeptides to increase/decrease food intake
50
Q

Describe the ob/ob mouse experiment.

A
  • mouse with mutation meaning it could not produce the hormone leptin
  • this led to severe obesity in the mouse - eats excessively
  • developed high blood sugar, pancreatic islet cell enlargement and increased insulin levels
51
Q

What is leptin?

A
  • a hormone made by white adipose tissue and enterocytes in small intestines
  • circulates in plasma
  • regulates appetite (food intake) and thermogenesis (energy expenditure)
52
Q

Where does leptin act?

A

Acts upon receptors in the arcuate and ventromedial hypothalamic nuclei

53
Q

What roles in disease development does leptin play? (3)

A
  • development of atherosclerosis through innate immune system, especially through complement system
  • low levels in Alzheimer’s disease
  • depression associated with low levels of leptin
54
Q

Describe the overall systemic effects of leptin. (4)

A
  • low when low body fat
  • high when high body fat
  • replacement of leptin in ob/ob mouse decreases weight
  • hormone that decreases food intake and increases thermogenesis (energy expenditure)
55
Q

What is congenital leptin deficiency?

A
  • incredibly rare genetic condition that causes severe obesity very early in life due to low serum leptin
  • born with a normal weight but constantly hungry and quickly gain weight
  • only few people known to have defect
56
Q

What are leptin levels like in obese patients?

A
  • serum leptin is significantly higher in obese subjects than normal weight people
  • serum leptin is correlated with % of body fat of subjects
  • this suggests that most obese people are resistant to endogenous leptin production
57
Q

What are the three main mechanisms through which the physiological effect of leptin may not work?

A
  • insufficient production
  • defective leptin receptor signalling/regulatory defect –> reduced/normal leptin level despite high adipose tissue mass
  • decreased sensitivity to leptin (similar to insulin resistance in T2DM) –> inability to detect satiety despite high energy stores and leptin levels
58
Q

How do leptin levels relate to fat mass, and what does this have to do with leptin resistance?

A
  • leptin circulates in plasma in concentrations proportional to fat mass
  • overweight humans have more leptin
  • this proves that leptin resistance is a thing
59
Q

What does leptin resistance cause?

A

Obesity - hormone (leptin) is present but does not signal effectively

60
Q

How effective is leptin as a weight control drug?

A

Not effective

61
Q

Why do we feel less hungry after a meal?

A
  • bulk in stomach? no
  • nutrients in circulation? limited
  • hormonal signals from gut!!
62
Q

What secretes GI (gut) hormones?

A

Secreted by enteroendocrine cells in the stomach, pancreas and small bowel

63
Q

What do GI hormones control?

A

Various functions of digestive organs e.g. motility, appetite, satiety, salivation etc

64
Q

What are the two most important hormones involved in appetite regulation, and what do they do?

A
  • ghrelin - stimulates appetite, increases gastric emptying
  • peptide tyrosine tyrosine (PYY) - inhibits food intake
65
Q

When are blood ghrelin levels highest and why?

A
  • before meals to help prepare for food intake by increasing gastric motility and acid secretion
  • returns to lower levels after meals
66
Q

What is the name ‘ghrelin’ based on?

A

Based on its role as a Growth Hormone RELeasing peptide (GHREL)

67
Q

What is ghrelin also known as?

A

Hunger hormone because it increases food intake

68
Q

How does ghrelin work in the hypothalamus?

A
  • directly modulates neurons in the arcuate nucleus
    • stimulates NPY/AGRP neurons
    • inhibits POMC neurons
69
Q

What are the roles of ghrelin? (2)

A
  • increases appetite
  • involved in regulation of reward, taste sensation, memory and circadian rhythm
70
Q

What happens to ghrelin throughout the day (describe graph)?

A
  • plasma ghrelin levels increased nearly 2x immediately before each mealtime
  • falls to a trough around 1h after mealtime
  • intermeal ghrelin levels have a diurnal rhythm - rise throughout the day to a peak at 1am, then falls overnight to a low at 9am
71
Q

What else (apart from mealtime) do plasma ghrelin levels positively correlate with?

A

Age

72
Q

What is the effect of ghrelin on food intake levels?

A
  • more ghrelin means more cumulative food intake which was associated with excess weight gain and adiposity in mice
  • in humans, energy intake was a lot higher when ghrelin was given intravenously to subjects vs saline (they ate more from a buffet)
73
Q

What is peptide tyrosine tyrosine (PYY)?

A

Short peptide (36 amino acids) released in the terminal ileum and colon in response to feeding

74
Q

What does peptide tyrosine tyrosine (PYY) do?

A

Reduces appetite - can be digested or injected IV

75
Q

What causes peptide tyrosine tyrosine (PYY) release?

A

Food arriving in terminal ileum and colon

76
Q

What food types increase peptide tyrosine tyrosine (PYY) release? (3)

A
  • dietary fibres
  • wholegrains
  • enzymatic breakdown of crude fish proteins
77
Q

How does peptide tyrosine tyrosine (PYY) act on the hypothalamus?

A
  • inhibits NPY release
  • stimulates POMC neurons
78
Q

What is the effect of PYY on feeding in mice?

A
  • decreases food intake
  • the degree of PYY release from the GI tract postprandially is proportional to the calorie intake
79
Q

What is the effect of PYY on feeding in humans?

A
  • PYY infusions resulted in dose-dependent reduction in food and calorie intake with maximal inhibition of 35% compared to saline administration
  • fluid ingestion also reduced
  • side effects - especially in higher doses:
    • nausea
    • fullness
    • subjects also experiences less hunger and early fullness in premeal period during PYY infusions
80
Q

What comorbidities is obesity associated with? (10)

A
  • depression (1/3 with BMI>35)
  • stroke
  • myocardial infarction
  • sleep apnoea (swollen airways –> sleep apnoea –> tiredness –> affects reward mechanism –> increased food intake)
  • hypertension
  • diabetes
  • bowel cancer
  • osteoarthritis (joints need to carry more weight)
  • peripheral vascular disease
  • gout
81
Q

What do obesity trends correlate with?

A

High obesity rates cause high hospital admissions

82
Q

How do environmental and genetic variance interact in obesity?

A
  • only in the presence of a toxic environment that genetic susceptibility is expressed as the disease phenotype
  • toxic environment = genetically prone possess disease phenotype, but not in genetically resistant population

Year 2 - BRS (84 decks)

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