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BIOL31571 > Lecture 9 - ACTH and Glucocorticoids- the regulators of stress responses > Flashcards

Lecture 9 - ACTH and Glucocorticoids- the regulators of stress responses Flashcards

1
Q

HPA axis: what is it, what do each of the parts release, and what do these secreted hormones do?

A

Hippocampus - pituitary gland - adrenal gland

The hippocampus releases corticotrophin-releasing hormone (CRH) which activates the pituitary gland

Pituitary gland - releases adrenocorticotrophic hormone which activates the adrenal gland

Adrenal gland - releases cortisol which affects the body

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2
Q

Glucocorticoids: what is an example of a difference between humans and rats/mice?

A
  • Cortisol in humans
  • Corticosterone in rats and mice
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3
Q

Hypothalamus and pituitary locations

A

Hypothalamus sits behind the eye with the pituitary gland just below it, connected by the infundibulum, a stalk of nerves and blood vessels connecting the posterior parts

The pituitary gland sits just below the optic chiasm and just above the sphenoid sinus

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4
Q

Infundibulum

A

Pituitary stalk

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5
Q

Hormones produced by the adrenal gland: where are they produced, what are the types, and what are examples of them?

A

Cortex:
* Glucocorticoids - cortisol
* Mineralocorticoids - aldosterone
* Sex steroids - testosterone/oestrogen

Medulla:
* Epinephrine
* Norepinephrine

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6
Q

Glucocorticoid effects: liver, adipose tissue, muscle, immune system, bone, brain, cardiovascular system, kidney, skin, and fetus

A
  • Liver - Increases blood glucose - stimulates gluconeogenesis and glycogenolysis
  • Adipose tissue - increase lipolysis
    which go to the liver
  • Muscle - decreases protein synthesis and increases protein metabolism
  • Immune system - anti-inflammatory and immunosuppressive effects
  • Bone - decrease osteoblasts and stimulate bone resorption
  • Brain - affect memory and sleep patterns and mood
  • CV system - increase blood pressure and cardiac output
  • Kidney - increase water diuresis and glomerular filtration rate, minor effect on sodium retention and potassium
    excretion
  • Skin - inhibit keratinocyte proliferation and
    differentiation and reduce sebum production
  • Fetus - required for organ maturation particularly the lung
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7
Q

Glucocorticoids: what are their effects on the liver?

A

Liver - Increases blood glucose - stimulates gluconeogenesis and glycogenolysis

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8
Q

Glucocorticoids: what are their effects on the adipose tissue?

A

Adipose tissue - increase lipolysis
which go to the liver

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9
Q

Glucocorticoids: what are their effects on the muscles?

A

Muscle - decreases protein synthesis and increases protein metabolism

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10
Q

Glucocorticoids: what are their effects on the immune system?

A

Immune system - anti-inflammatory and immunosuppressive effects

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11
Q

Glucocorticoids: what are their effects on the bones?

A

Bone - decrease osteoblasts (inhibiting bone formation) and stimulate bone resorption

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12
Q

Glucocorticoids: what are their effects on the brain?

A

Brain - affect memory and sleep patterns and mood

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13
Q

Glucocorticoids: what are their effects on the cardiovascular system?

A

CV system - increase blood pressure and cardiac output

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14
Q

Glucocorticoids: what are their effects on the kidneys?

A

Kidney - increase water diuresis and glomerular filtration rate, minor effect on sodium retention and potassium
excretion

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15
Q

Glucocorticoids: what are their effects on the skin?

A

Skin - inhibit keratinocyte proliferation and
differentiation and reduce sebum production

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16
Q

Glucocorticoids: what are their effects on the fetus?

A

Fetus - required for organ maturation particularly the lung

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17
Q

Glucocorticoids: how do they affect insulin?

A

They result in glucose production from the liver - initially suppressing insulin to raise blood glucose levels

Once blood glucose levels have been raised, this acts back on the pancreas, causing insulin secretion which causes the recruitment and storing of glucose in tissues such as muscles, supplying them with the glucose they need for the stressful situation they are in

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18
Q

Is the immunosuppressive nature of glucocorticoids always bad?

A

No, it is only bad when it is uncontrolled

Stopping inflammation is important in not having excessive inflammation and damage to tissues and the body

19
Q

Gluconeogenesis

A

Producing glucose from non-carbohydrate sources (proteins etc)

20
Q

Glycogenolysis

A

Breaking down glycogen into glucose

21
Q

Lipolysis

A

Metabolic process that breaks down fat stores into energy-rich fatty acids and glycerol

22
Q

Water diuresis

A

Increased urine flow caused by decreased reabsorption of solute-free water in the collecting ducts

23
Q

Mechanisms controlling the HPA axis

A
  • Circadian - ACTH/cortisol vary on time
  • Pulsatile -
  • Stress - promotes CRH release
24
Q

Circadian rhythm: what is it, how is it different to a diurnal rhythm, and how can it be related to the HPA axis

A

The natural 24-hour cycle of physical, mental, and behavioural changes that occur in the body

Diurnal rhythm - 24-hour cycle synchronized to and dependent on an external cue
Circadian rhythm - 24-hour cycle based on internal, cyclic events (synchronised to but not dependent on an external cue)

Diurnal Rhythm - ACTH and cortisol levels are highest at ~06.00 and lowest at ~00:00

25
Q

Pulsatile control of HPA axis hormones

A

Episodes of release last from 1 to 3 hours
* 7 to 8 episodes per 24 hours.
* They are not evenly distributed, there are fewer episodes at night
* Reason for episodic release of ACTH and cortisol is not clearly understood but recent computational modelling suggests timeframe of molecular events controls it

26
Q

HPA axis negative feedback

A

Cortisol inhibits the secretion of ACTH from the pituitary as well as CRH from hippocampus

27
Q

Factors controlling the HPA axis: what are they and how do they affect the HPA axis?

A
  • Interleukins - stimulate HPA axis which in turn suppresses the immune system as glucocorticoids exhibit their effects
  • SME - very strongly activates the pituitary gland, causing high levels of ACTH production
  • CRH - stimulates ACTH weakly alone but strongly with AVP, suggesting a synergistic effect
  • AVP - stimulates ACTH weakly alone but strongly with CRH, suggesting a synergistic effect
28
Q

Factors controlling the HPA axis: what are they and how do they affect the HPA axis? (ER)

A

Inhibitors of CRH:
* L-dopa
* Serotonin
* VIP
* ANP
* GABA

Factors directly affecting the pituitary:
* PACAP
* LIF
* IL-1/2/6
* Oncostatin M
* Catecholamines

29
Q

SME: what is it, where is it obtained from, and what does it do?

A

Stalk median eminence - tissue obtained from the infundibulum, so contains the factors leaving the hypothalamus

Greatly activates the pituitary gland, causing high levels of ACTH production

30
Q

CRH: what is it, what is it synthesised by, where is it found, what does it do, what is its structure, and what is its receptor?

A

Corticotrophin Releasing Hormone

Synthesised by hypothalamus

  • Skin, immune cells, and adrenal gland in small amounts

Stimulates ACTH synthesis

41 amino acid peptide

  • CRH-R1 (accounts for all HPA activity)
  • CRH-R2
31
Q

AVP: what is it, what does it do, and how does it affect the HPA axis?

A

Arginine vasopressin - ADH

Controls water reabsorption

Simulates ACTH weakly alone but strongly with CRH, suggesting a synergistic effect

32
Q

ACTH production: what is the gene it originates from, how may it be regulated, and what proteins are integral to its processing?

A

POMC (Pro-opiomelanocortin) gene

May be regulated at POMC transcription, POMC mRNA translation, or POMC protein processing

Prohormone convertase 1

33
Q

POMC gene: what are the potential products from processing?

A
  • ACTH - adrenocorticotrophic hormone
  • βLPH - beta lipotrophin
  • N-POC - N-terminal pro-opiocortin
  • JP - Joining peptide
  • MSH- melanocyte-stimulating hormone
  • CLIP- corticotrophin-like intermediate peptide
  • βEP- beta-endorphin
34
Q

POMC processing: what are the reactions and what enzymes are key in the processing?

A

POMC —(PC1)–> βLPH + pro-ACTH

pro-ACTH —(PC1)—> JP + N-poc + ACTH

N-poc —(PC2)—> γ₃MSH

ACTH —(PC2)—> αMSH

βLPH —(PC2)—> βEP + βMSH

35
Q

Regulation of the POMC gene

A

POMC transcription promotors:
* CRH - CRHR activation, adenylyl cyclase activated, cAMP produced, PKA activated, cAMP response element binding protein activated, ChREBPB activated, promoting POMC transcription
* CRH - CRHR activation, MAPK pathway activated, downstream AP-1 promotes POMC transcription
* AVP - V1b (receptor) activated, cAMP produced, aiding the CRH activation
* AVP - V1b activated, PKC activated, unknown further mechanisms

POMC transcription inhibitors:
* Glucocorticoids - bind to GR which translocates into the nucleus and inhibits POMC transcription
* Glucocorticoids - GR activated which then inhibits K⁺ channel, preventing the influx of Ca²⁺ which causes ACTH release

36
Q

Regulation of the POMC gene (ER)

A
  • ERK/Nur77 pathway
  • K⁺ regulation controls membrane potential and promotes calcium release as K⁺ are released, Ca²⁺ influx promotes ACTH secretion
37
Q

Regulation of ACTH secretion: what are the two types of secretion and what are the mechanisms behind them?

A

Constitutive secretion:
* Immature secretory granule containing unprocessed POMC which is constantly secreted to maintain baseline POMC levels even without an external stress signal

Regulated secretion:
* Vesicles containing ACTH that has had the proper processing are produced from the Golgi and secreted in response to a secretagogue (ie CRH)

38
Q

ACTH: what receptor does it act on?

A

Melanocortin 2-Receptor (MC2-R)

39
Q

αMSH: what is it, why does its mutation in children result in obesity, what is it produced by, and what other adverse effects may it have?

A

α melanocyte-stimulating hormone

  • αMSH acts back on MC4R and MC3R receptors in the hypothalamus to inhibit hunger
  • If mutated, αMSH may fail to be produced and therefore children feel constant hunger and become obese

PC2 cleaving ACTH

In excess amounts, it may cause pigmentation as it can also bind to MC1R/MC5R receptors

40
Q

αMSH: what are the two receptor systems it can act on?

A

MC4R/MC3R in the hypothalamus - results in satiety and reduced hunger
MC1R/MC5R in the skin - results in pigmentation

41
Q

Cortisol: what is it produced from, what hormone stimulates its synthesis, what does it act on, at what times are its levels highest/lowest, and how does it travel around the body?

A

The zona fasciculata of the adrenal gland

ACTH from the pituitary gland

Sugar and stress

  • Negative feedback on the pituitary gland and hippocampus - inhibiting CRH and ACTH synthesis and secretion
  • The body’s glucocorticoid receptors

Highest - 6:00
Lowest - 00:00

Circulating cortisol is bound to a carrier protein - corticosteroid binding globulin (CBG)

42
Q

CBG: what is it, what does it do, how is it affected in certain diseases, and why is it so important?

A

Corticosteroid binding globulin

Binds circulating cortisol (responsible for binding 90% of cortisol and 60% of aldosterone)

CBG levels increased by diseases including
hyperthyroidism and diabetes, which will change the bioavailability of cortisol as only free cortisol is active

43
Q

Cholesterol synthesis and secretion in adrenal gland cells

A
  • Cholesterol is taken into the mitochondria through the StAR protein
  • It is then converted to pregnenolone
  • Pregnenolone moves into the ER where it is converted to 11-deoxycortisol which then moves back into the mitochondria where it is converted into cholesterol and can then be released from the cell

Why does this happen - who knows

44
Q

Cholesterol synthesis and secretion in adrenal gland cells (ER)

A

More in-depth image in the lecture

BIOL31571 (17 decks)

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