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Biochemistry Exam 2 > Lecture 12 : Cell Signalling Pathways Glucocorticoids, Estrogen, Progesterone and Testosterone > Flashcards

Lecture 12 : Cell Signalling Pathways Glucocorticoids, Estrogen, Progesterone and Testosterone Flashcards

1
Q

How are receptors grouped?

A

Grouped based on the receptor they bind to.

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2
Q

What are all steroid hormones synthesized from?

A

Cholesterol

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3
Q

What is unique about steroid hormones?

A

Steroid Hormones are lipids, which are fat soluble. As such steroids can pass freely by diffusion through biological membranes and enter cells without a specific transporter mechanism

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4
Q

How does cholesterol circulate in the blood?

A

Because of a steroid’s lipid or hydrophobic properties,

  • steroid hormones circulate bound to specific binding or carrier proteins rather than circulating free.
    • For example, sex-hormone binding globulin or corticosteroid-hormone binding globulin.
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5
Q

How do steroids exert their biological effects on cells?

A

Via two routes:

  • Slower genomic response (hours and longer)
  • Faster nongenomic mechanism (minutes)
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6
Q

What mediates the genomic actions?

A

Nuclear receptors

•Nuclear receptors mediate genomic actions with time frames on hours to days.

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7
Q

What do Membrane-associated receptors do?

A

Membrane-associated receptors activate intracellular signaling pathways to bring about NONGENOMIC actions of steroid hormones.

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8
Q

Cholesterol Pathway

and

Molecule

A
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9
Q

Steroid Hormones

A
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10
Q

Why is estrogen unique?

A

It has an aromatic structure to the A ring,

it gets made by the action of the enzyme of aromatase (aromatization)

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11
Q

Biosynthesis of Cholesterol to Major Steroid Hormones

A

Don’t need to know the enzymes,

EXCEPT FOR AROMATASE

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12
Q

Concentration of Steroid Hormones in the Blood for Men and Women

A
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13
Q

What do Plasma Proteins do?

A

Plasma proteins bind and facilitate the circulation of lipid like (hydrophobic) hormones

  • Examples:
    • Retinoic acid binding protein binds retinoic acid
    • Sex hormone binding globulin binds testosterone and estradiol
    • Vitamin D binding protein binds vitamin D
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14
Q

What is Retinoic Acid?

A

Is a lipid-soluble hormone that is derived from Vitamin A1

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15
Q

What is synthesized from Tyrosine residues that are in Thyroglobulin

A

Thyroxine

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16
Q

What are the steps in Steroid Hormone Action?

A

Genomic Mechanism

(direct action of S bound to its receptor acting on a response element in the DNA)

  • Steroid Hormone (S) diffuses through Plasma Membrane
  • S can bind to Cytoplasmic Hormone Receptor (HR) and that gets translocated into the nucleus
  • or
  • There’s evidence now that the SH can go into the nucleus and bind to Resident HR

OR

Nongenomic Mechanism

(Membrane-bound receptor)

  • S can behind to Plasma Membrane HR
  • That leads to a Second Messenger
  • That leads to changes in cell signalling
  • Then some of those changes can result in factors that get translocated into the nucleus and alter gene expression
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17
Q

Structure of Nuclear Steroid Hormone Receptors

A

All have DNA binding domain and hormone-binding domain (the two most important regions)

Needs both to have a functional steroid hormone receptor

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18
Q

How do Nuclear Steroid Receptors bind DNA?

A

Hormone receptors recognize a specific sequence of nucleotides in DNA, only bind to certain regions of the DNA (b/c these sequences are only found with their target genes which are what is going to regulate the transcription of)

Referred to as Nuclear Response Element Sequences

(These receptors look for specific sequences of DNA)

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19
Q

Where are Glucocorticoids Synthesized?

A

In the Adrenal Cortex

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20
Q

Where do Glucocorticoids bind?

A

Glucocorticoids binds to the GC receptor

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21
Q

Glucocorticoid =?

A

Glucose + Cortex + Steroid,

  • derived from its role in the regulation of metabolism of glucose
  • Synthesis in the adrenal cortex
  • Steroidal Structure
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22
Q

What do Glucocorticoids do?

A

Bind to specific receptor and stimulate transcription of anti-inflammatory proteins and factors.

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23
Q

What is Cortisol?

A

Cortisol is a natural steroid hormone, more specifically a glucocorticoid.

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24
Q

What produces Cortisol?

A

Cortisol is produced by the Zona Fasciculata of the Adrenal Cortex.

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25
Q

When is Cortisol released?

A

Cortisol is released in response to stress and a low level of blood glucose.

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26
Q

What are the primary functions of Cortisol?

A
  • Increase blood sugar through gluconeogenesis
  • Suppress the immune system
  • Aid the metabolism of fat, protein, and carbohydrate
  • Decreases bone formation by causing osteocyte apoptosis (or autophagy at lower doses) as a side effect
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27
Q

How does Cortisol decrease bone formation?

A

Cortisol decreases bone formation by causing osteocyte apoptosis (or autophagy at lower doses) as a side effect

Cortisol causes apoptosis of cells (particularly osteocytes) when used at high enough doses

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28
Q

Osteocyte Apoptosis does what?

A

Can trigger a reduction in bone density by stimulating osteoclast formation.

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29
Q

What is one of the problems encountered in the chronic use of glucocorticoids?

A

Glucocorticoid induced Osteoporosis

(Glucocorticoid Osteoporosis GIO)

competes w/ treating conditions that need glucocorticoids while balancing those against the fact that it may have a negative consequences on the skeleton

30
Q

How are Glucocorticoids used?

A
  • Can be used in low doses in adrenal insufficiency.
  • In much higher doses, oral or inhaled glucocorticoids are used to suppress various allergic, inflammatory, and autoimmune disorders.
    • Inhaled glucocorticoids are the second-line treatment for asthma.
  • They are also administered as post-transplantation as immunosuppressants to prevent acute transplant rejection and the graft-versus-host disease.
    • They don’t prevent the infection though, but they do also inhibit later reparative processes.
31
Q

How is Glucocorticoid Synthesis regulated?

A

Glucocorticoids synthesis is regulated by corticotrophin-releasing hormone by nerves in the hypothalamus

  • What this ultimately does is, it stimulates the production of ACTH which acts on the adrenal cortex to produce and release cortisol.
32
Q

What is the Nuclear Mechanism of Glucocorticoids?

A
  1. Transported in the blood and diffuse across the membrane.
  2. Bind to a cytoplasmic receptor
    1. Cytoplasmic receptor exists in a complex with heat shock proteins.
  3. Binding of the Hormone to the Cytoplasmic Receptor causes the Heat-shock protein to dissociate. Then Two of the Cytoplasmic Receptors Diamerize.
  4. Dimerization leads to binding in the nucleus to the Glucocorticoid Response Element (GR````That Cytoplasmic Receptor from before’’’’) and this results in changes in gene expression
33
Q

What is one of the main functions of cortisol?

A

To increase Gluconeogenesis by the liver.

Also has effects on the following:

  • Muscle
  • Adipose Tissue
  • Brain
  • Bone
  • CVS (Cardiovascular System)
  • Immune System
  • Kidney
  • Skin/Connective Tissue
  • Fetus
34
Q

What is the effect of Cortisol on Muscle?

A

Cortisol in Muscle causes the break down of proteins into amino acids

  • This can then circulate in the blood and be taken up by the liver which can then be a substrate for further gluconeogenesis.
35
Q

What is the effect of Cortisol on Adipose tissue?

A

Cortisol can stimulate pre-fatty acid release from Adipose Tissue to produce fatty acids.

  • Fatty acids can then be used in the liver to produce acetyl CoA and synthesis of Glucose.
36
Q

How do Glucocorticoids alter or regulate Inflammatory and Immune response?

A

Inflammatory Response

  • Formation of Arachidonic Acid
  • Arachidonic Acid gets converted into Prostagladins, Thromboxanes, and Leukotrienes.
    • Glucocorticoids (GC) induce the formation of Lipocortin.
    • Lipocortin is an inhibitor of Phospholipase A2 (PL-A2).
      • PLA2 is what converts Phosphatidyl Choline into Arachidonic Acid.
    • This means the formation of Arachidonic Acid gets blocked.
    • GC also inhibit the formation of COX1 and COX2.
      • COX1 and COX2 and what convert Arachidonic Acid into Prostaglandins and Thromboxanes.
  • GC also inhibit the step of Leukotrienes which stimulates Phagocytosis.

Immune Response

  • GC prevents the production of Interlukin 1Beta IL-1B which is normally produced by Macrophages.
    • IL-1B is responsible in Fever production (the normal response of the body to infection)
    • IL-1B is important for T-Cell Activation
  • GC block T-cell activation of B-cells

Glucocorticoids work on multiple levels.

Long Explanation, starts at 22:40

37
Q

What’s a good way to knock down periodontitis, a bad inflammation?

A

A Glucocorticoid is a good way to knock that down.

38
Q

What do GCs inhibit in the Inflammatory response?

A

In the Inflammatory Response,

  • GC induces Lipoproteins which inhibit PLA2(Phospholipase A2) which would then mean that Arachidonic Acid can’t be made from Phosphatidyl Choline.
  • GC also inhibit the COX1&2 which is the enzyme responsible for turning Arachidonic Acid into Prostaglandins and Thromboxanes
  • GC also inhibits the step of Leukotienes which is responsible for Phagocytosis.
39
Q

What do GCs inhibit in the Immune Response?

A

Immune Response

  • GC prevents the production of Interlukin 1Beta IL-1B which is normally produced by Macrophages.
    • IL-1B is responsible in Fever production (the normal response of the body to infection)
    • IL-1B is important for T-Cell Activation
  • GC block T-cell activation of B-cells
40
Q

What is the Mechanism of Non-Steroidal Anti-Inflammatory Drugs on Prostaglandin Synthesis?

A
  • Inhibits COX1 and COX2
    • Prevents production of Prostaglandins and Thromboxanes from Arachidonic Acid through a Nonsteroid Mechanism of Action.
41
Q

Explain the mechanism behind Sex Hormone Action

A
  1. Sex Hormone action has a hypothalamus pituitary-gonadal axis of control.
  2. Releasing Hormone stimulates the pituitary to produce either Follicle Stimulating Hormone (FSH) or Leutinizing Hormone (LH).
  3. When either FSH or LH is produced, they will act on the Gonads that then produce the sex steroids (hormones).
    1. Sex hormones are necessary for secondary characteristics and for the formation of gametes.
  4. Sex Hormones have actions on many different tissues.
  5. Sex hormones feedback to the level of the Pituitary or Hypothalamus.
    1. Long Feed Back Loop.
42
Q

What is Osteoporosis?

A

Osteoporosis is a skeletal disorder that is characterized by compromised bone strength.

43
Q

What does bone strength primarily reflect?

A

Bone strength primarily reflects the integration of bone quality and bone density.

44
Q

What are the results of Osteoporosis?

A
  • 1.5M Bone Fractures
  • Hip, Vertebral, Wrist & other Fractures
45
Q

What are the annual consequences of Hip Fractures?

A
  • 24% will die from complications
  • 25% will require long-term care
46
Q

What percent of postmenopausal women on average will suffer at least one osteoporotic fracture?

A

50%

47
Q

What are the effects of Estrogen on Bone Mass Density (BMD) and Fractures?

A

Estrogen is important for maintaining bone.

Changes in Bone Mass Density at Menopause

  • Bone loss in women begins about two years prior to last menses.
  • Estrogen-deprivation bone loss is completed over 6 years.
  • Estrogen-deprivation bone loss ranges from 6% to about 12%
    • -1 standard deviation = osteopenic
    • -2.5 or below = osteoporotic
    • The range b/w -1 and -2.5 where we try to maintain the skeleton if at all possible
48
Q

How does Osteoporosis affect the jaw?

A

Individuals that have low bone density may be more susceptible to alveolar or bone loss associated with Periodontitis.

49
Q

What is the alveolar bone associated with?

A

The Dentition.

50
Q

What happens to the alveolar bone when there’s a decrease in bone density?

A

It undergoes the same kinds of changes that normal bone undergoes in the skeleton with respect to Osteo Porosis.

51
Q

When is Osteoporosis important in a clinical environment?

A

If you know they have osteoporosis, they may not have good enough quality bone to allow for an implant to be stable.

52
Q

What are does SERMS stand for?

A

Selective Estrogen Receptor Modulators

53
Q

What are drugs are used for Osteoporosis?

A

SERMS

=

Selective Estrogen Receptor Modulators

These bind to the receptors

40:00

54
Q

What are Progesterone levels in females like?

A
  • During monthly cycle, progesterone and estrogen levels are low.
  • LH and FSH begin to increase right at the point of ovulation roughly mid cycle.
  • Then go into the Leutial faze where Progesterone levels spike in order to maintain implantation if the egg is fertilized.
    • If not, it goes back down.
  • During Pregnancy, both Estrogen and Progesterone levels are maintained at fairly high levels up until birth and then they come back down.
55
Q

What are progesterone levels like in males?

A

Males maintain relatively constant, low levels of progesterone.

56
Q

What are the Androgens that can be converted into Estrogens?

A
  • Dehydroepiandrosterone (DHEA)
  • Androstenediol
  • Androstenedione
  • Testosterone (T)

Because they are Aromaticable?

41:40

57
Q

Which Androgen CAN NOT be converted into an Estrogen and why?

A
  • 5α-Dihydrotestosterone (DHT)
    • Because it is NOT Aromatisable
58
Q

What are some Clinical uses for Androgens?

A
  • Can be used for Male Androgen Insufficiency syndrome.
  • Treatment of children with growth failure
  • Bone marrow stimulation in certain diseases resulting in hypoplastic and aplastic anemia
  • Masculinizing hormone therapy
  • Many others, use of anabolic steroids in athletes, etc…
59
Q

What are Anabolic Steroids?

A

Anabolic Steroids are synthetic variants of testosterone.

60
Q

What are Anabolic Steroids used to treat?

A

Anabolic steroids are used therapeutically to:

  • Induce male puberty
  • Treat chronic wasting conditions such as cancer and AIDS
61
Q

What are the health risks associated with the use of Anabolic Steroids?

A
  • Harmful changes in Cholesterol levels,
  • Acne,
  • High blood pressure,
  • Liver Damage
  • Changes in the Heart (Left Ventricle of the heart)
  • Can cause psychiatric symptoms including:
    • increased aggression,
    • violence
    • mania
  • less frequently associated with psychosis
  • Increased incidence of suicide associated with steroid abuse
    • in weight lifters, WWE wrestlers
62
Q

What are some diseases associated with Steroid Hormone Receptors?

A
  • Androgen Insensitivity Syndrome
  • Estrogen Receptors
  • Glucocorticoid Receptors
  • Vitamin D Receptor

45:00

63
Q

What is Androgen Insensitivity Syndrome?

A

Androgen Insensitivity Syndrome involves mutations in the hormone-binding region which causes absence of hormone binding or qualitative/quantitative changes leading to testicular feminization or Reifenstein syndrome

64
Q

Why are women generally shorter than men?

A

Women are generally shorter than men because when they have regular menses, they get their spike in estrogen levels and that shuts down their epiphysis and they no longer grow vertically while that does not happen in males until a little bit later.

65
Q

What would a mutation in the ESR1 gene do?

A

….?

66
Q

What are some nongenomic mechanisms of Steroid Hormones?

A
  1. Activating Protein Kinase C (PKC) or cAMP
  2. Induces formation of binding elements that then act on the DNA
  3. Activating Protein Kinase C (PKC) or cAMP also have cytoplasmic effects that involve things like AKT signalling and the MAP Kinase (MAPK) pathway
67
Q

What are Agonists?

A

Agonists stimulate

  • they bind to a steroid hormone receptor and trigger signalling pathway
68
Q

What are Antagonists?

A

Antagonists Inhibit

Antagonists can bind to the steroid hormone receptor and prevent downstream signalling

69
Q

Summary

A
70
Q
A

Biochemistry Exam 2 (7 decks)

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