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BRS Flashcards (Y2) > Appetite > Flashcards

Appetite Flashcards

1
Q

What three factors determine when we get thirsty?

A

Body fluid osmolality
Blood volume is reduced
Blood pressure is reduced

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2
Q

What is the most potent stimulus for drinking?

A

Plasma osmolality increase is the more potent stimulus – 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 response

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3
Q

How is plasma osmolality regulated?

A

Regulated by ADH
Acts on the kidneys to regulate the volume & osmolality of urine
Increases Aquaporin 2 channels in collecting duct
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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4
Q

What are osmoreceptors and where are they found?

A

Sensory receptors
Involved in osmoregulation
Found in the hypothalamus

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5
Q

Where are osmoreceptors found in the hypothalamus?

A

Organum vasculosum of the lamina terminalis (OVLT)
Subfornical Organ (SFO)

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6
Q

How do osmoreceptors stimulate ADH release?

A

Cells shrink when plasma more concentrated
Proportion of cation channels increases – membrane depolarizes
Send signals to the ADH producing cells to increase ADH
Causes fluid retention and invokes drinking

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7
Q

What happens to thirst sensation when you drink and what receptors are involved?

A

Thirst is decreased by drinking even before sufficient water has been absorbed by the GI tract to correct plasma osmolality
Receptors in mouth, pharynx, oesophagus are involved
Relief of thirst sensation via these receptors is short lived

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8
Q

When is thirst completely satisfied?

A

Once plasma osmolality is decreased
or
Once blood volume/arterial pressure is corrected

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9
Q

How is blood pressure/volume regulated and how does this link to thirst?

A

Decrease in BP detected by juxtaglomerular cells of renal afferent arteriole
Stimulates release of renin -> renin catalyses conversion of angiotensinogen to angiotensin I -> ACE converts AT1 to AT2
AT2 - stimulates thirst, aldosterone release, ADH secretion, vasoconstriction (increased sympathetic activity)

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10
Q

Briefly explain body weight homeostasis

A

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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11
Q

What hormones are involved in appetite regulation?

A

Ghrelin, PYY and other gut hormones
Leptin
Neural input from periphery and other brain regions

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12
Q

What do the terms orexigenic and anorectic mean?

A

Orexigenic - appetite stimulant
Anorectic - appetite suppressive

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13
Q

What is the arcuate nucleus and how is it adapted for its function?

A

Brain area involved in the regulation of food intake
Incomplete blood brain barrier - allows access to peripheral hormones
Integrates peripheral and central feeding signals

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14
Q

What two neuronal populations are found in the arcuate nucleus?

A

Stimulatory (NPY/AGRP neuron)
Inhibitory (POMC neuron)

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15
Q

What effect does leptin have on NPY/AGRP?

A

Inhibitory

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16
Q

By what mechanism do AGRP and POMC affect appetite respectively?

A

Neurons project directly to paraventricular nucleus (PN) of hypothalamus:
- AGRP inhibits MC4R release from PN
- POMC stimulates release of alpha-MSH -> stimulates MC4R release
MC4R decreases food intake

17
Q

What is a lack of NPY/AGRP mutations associated with in humans?

A

Appetite

18
Q

What may POMC deficiency and MC4-R mutations cause?

A

Morbid obesity

19
Q

Are CNS mutations responsible for the prevalence of obesity?

A

No - but help to explain how signaling works

20
Q

Is the control of appetite localised in the hypothalamus?

A

No, other brain/CNS regions are involved
Amygdala - rewards centres, emotion may affect appetite
Vagus nerve -> brain stem -> hypothalamus

21
Q

What is adipostat and how does it affect food intake?

A

Circulating hormone produced by fat
Hypothalamus senses hormone concentration and then alters neuropeptides to increase or decrease food intake

22
Q

What is leptin and where is it made?

A

Hormone that circulates in plasma
Made in adipocytes of white adipose tissue and enterocytes

23
Q

What effect does leptin have on the hypothalamus?

A

Acts on hypothalamus to regulate appetite and thermogenesis (energy expenditure)
Decrease appetite, increases expenditure

24
Q

How do leptin levels vary with body fat?

A

Low when body fat is low
High when body fat is high
Circulates in plasma in concentrations proportional to fat mass

25
Q

What is observed in children with congenital leptin deficiency and how are they treated?

A

Extremely obese
Leptin replacement has been effective in reducing body weight
Very rare

26
Q

If humans with more body fat have higher leptin, how comes people still become obese?

A

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

27
Q

Is leptin effective as a weight control drug?

A

No

28
Q

Why do we feel less hungry after a meal?

A

Mainly due to hormonal signals from the gut

29
Q

Where are GIT hormones secreted from?

A

Enteroendocrine cells in stomach, pancreas and small bowel

30
Q

When are ghrelin concentrations highest in the blood and why?

A

Before meals - helps prepare for food intake by increasing gastric motility (increases gastric emptying) and acid secretion

31
Q

What is the mechanism of action of ghrelin?

A

Stimulates NPY/Agrp neurons
Inhibits POMC neurons
Increases appetite

32
Q

Aside from appetite, what else is ghrelin involved in?

A

Regulation of reward, taste sensation, memory, circadian rhythm

33
Q

What is peptide tyrosine tyrosine (PYY)?

A

Short peptide released in terminal ileum (TI) and colon in response to feeding (36 amino acids)
Food arriving in TI or colon stimulates release

34
Q

What does peptide YY do?

A

Reduces appetite
Inhibits NPY release and stimulates POMC neurons

35
Q

What are some consequences of obesity?

A

Associated with comorbidities, e.g. stroke, MI, hypertension, diabetes, sleep apnoea and depression

36
Q

Describe the interaction between environment and genetic variance in the prevalence of obesity/overweight phenotypes

A

BRS Flashcards (Y2) (79 decks)

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