Appetite Flashcards

1
Q

what is thirst controlled by?

A
  1. Body fluid osmolality – this is the most potent stimulus
  2. Blood volume is reduced
  3. Blood pressure is reduced
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2
Q

what hormone regulates osmolality?

A
  • Antidiuretic hormone (ADH) or vasopressin- water reabsorption
  • Acts on the kidneys to regulate the volume & osmolality of urine
    • Collecting duct - Aquaporin 2 channel
  • 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).

ADH is stored in the posterior pituitary

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3
Q

where are osmoreceptors located?

A

in hypothalamus

  • Sensory receptors (osmoreceptors)
  • In organum vasculosum of lamina terminalis (OVLT) and sub fornical organ (SFO)
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4
Q

how do osmoreceptors affect ADH release?

A
  1. Cells shrink when plasma more concentrated
  2. Proportion of cation channels increases – membrane depolarizes
  3. Send signals to the ADH producing cells to increase ADH
  4. Fluid retention
  5. Invokes drinking
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5
Q

how is sensation of thirst decreased?

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.

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

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6
Q

describe the renin-angiotensin-aldosterone system and its effects

A
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7
Q

what types of medication is used to treat high BP?

A

ACEi and renin inhibitors

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8
Q

how is bodyweight homeostasis maintain?

A
  • The central circuit defend against reduction of body fat was revealed
  • A reduction in fat mass increases food intake and reduces energy expenditure
  • Adipose tissue expansion reduces food intake and increases energy expenditure
  • System against rapid expansion is yet to be discovered
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9
Q

how is appetite regulated?

A
  • Largely regulated in hypothalamus
  • Provides link between peripheral stimulus/hormones and upper control
  • Peripheral stimulus via vagus nerve to brain stem which communicates with hypothalamus
  • Hypothalamus communicates with other systems such as amygdala
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10
Q

how does the hypothalamus regulate appetite?

A
  • Signals can be orexigenic (stimulating) or anorexigenic (suppressing)
  • Arcuate nucleus= aggregation of neurons in medial basal part, adjacent to 3rd ventricle
    • Causes orexigenic and anorectic
  • Paraventricular nucleus
    • adjacent to 3rd ventricle
    • Neurons project to posterior pituitary (ADH storage)
    • Orexigenic and anorectic
  • Lateral hypothalamus = orexigenic peptides
  • Ventromedial hypothalamus= satiety (anorectic)
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11
Q

how does the arcuate nucleus control appetite and energy expenditure?

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
  • Two neuronal populations:
    • Stimulatory (NPY/Agrp neuron)
    • Inhibitory (POMC neuron)
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12
Q

what is the melanocortin system activated by?

A

products of POMC (& MSH)

  • MC4R are expressed in paraventricular nucleus
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13
Q

what mutations affect appetite?

A
  • No NPY or Agrp mutations associated with appetite discovered in humans.
  • POMC deficiency and MC4-R mutations cause morbid obesity.
  • Mutations not responsible for the prevalence of obesity - but useful to explain signaling.
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14
Q

what does leptin hormone do?

A
  • Decreases appetite (inhibitory)
  • Made by adipocytes in white tissue and enterocytes in small intestine
  • Circulates in plasma
  • Acts upon the hypothalamus decreasing appetite (intake) and increasing thermogenesis (expenditure)
  • It also in development of atherosclerosis through innate immune system
  • Low levels in Alzheimer’s and depression
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15
Q

what happens when leptin is missing?

A

missing in ob/ob mouse–> obesity

replacement decreases weight

  1. increased food intake
  2. energy expenditure
  3. fat and glucose metabolism
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16
Q

what happens in congenital leptin deficiency?

A
  • Sever obesity early in life
  • Constantly hungry
  • Low leptin despite being obese
  • Rare
17
Q

what is serum leptin conc correlated with?

A
  • Serum leptin concentration are correlated with percentage fat
    • Low when low body fat
    • High when high body fat
    • Obesity due to leptin resistance
      • Hormone present but doesn’t signal effectively
18
Q

can leptin be used as a weight control drug?

A

ineffective as weight control drug

19
Q

why do we feel less hungry after a meal?

A

hormone signals from gut

20
Q

what are the gastrointestinal appetite hormones secreted from?

A
  • Secreted by enteroendocrine cells in stomach, pancreas and small bowel
21
Q

what appetite hormones are released from the gut?

A

Ghrelin and Peptid YY

22
Q

what are the different hormones released from the GI tract?

A
23
Q

what are the effects of ghrelin?

A

stimulate appetite,

increases gastric emptying

24
Q

what are the effects of PYY?

A

inhibit food intake

25
Q

when are the levels of ghrelin highest?

A

before meals

  • help prepare for food intake by increasing gastric motility and acid secretion
26
Q

where does ghrelin act?

A
  • Directly modulates neurons in the arcuate nucleus
    • Stimulates NPY/Agrp neurons.
    • Inhibits POMC neurons.
27
Q

what are the other effects of ghrelin?

A
  • Regulation of reward, taste sensation, memory, circadian rhythm
28
Q

how do concentrations of ghrelin change through day?

A

Correlates with time of day (meal initiations)

29
Q

What are the effects of high ghrelin?

A

higher food intake

higher obesity

30
Q

where is PYY released from?

A
  • Short peptide released in the terminal ileum (TI) and colon in response to feeding (36 Amino acids)
31
Q

what are the effects of PYY?

A

reduces appetite

  • Food arriving to the TI and colon results in PYY release
  • Inhibits NPY release
  • Stimulates POMC neurons
32
Q

what are the effects of high PYY?

A

lower food intake= lower obesity

33
Q

what are the comorbidities of obesity?

A