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Biol 432 > Lecture 7 Midterm 1 > Flashcards

Lecture 7 Midterm 1 Flashcards

1
Q

what is the function of thyrotropin-releasing hormone (TRH)

A

regulation of thyroid stimulating hormone

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2
Q

what is the function of gonadotropin-releasing hormone

A
  1. (main) regulation of luteinizing hormone and follicle stimulating hormone from ant. pit
  2. limbic system (emotion) neuromodulator
  3. placenta and ovaries make GnRH - acts locally
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3
Q

somatostatin function

A

inhibition of GH, thyroid stimulating hormone, insulin and glucagon

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4
Q

growth hormone-releasing hormone function (GHRH)

A

stimulation of GH
- also tropic for somatotrophs (helps them grow/survive)

  • tropic = stimulates the release of another hormone
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5
Q

what is the prolactin-inhibiting hormone

A
  • dopamine

inhibits prolactin

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6
Q

corticotropin-releasing hormone (CRH)

A

produced in response to stress. Stimulates secretion of products derived from proopiomelanocortin (POMC) like adrenocorticotropic hormone (ACTH)

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7
Q

function of hypophysiotropic hormone

A

regulates the release of hormones from the ant pit; pulsatile

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8
Q

what do somatotrophs secrete and where from

A
  • growth hormone

- from ant pit

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9
Q

what do lactotrophs secrete and where from

A
  • prolactin

- from ant pit

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10
Q

what do thyrotrophs secrete and where from

A
  • thyroid-stimulating hormone (TSH)

- from ant pit

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11
Q

what do corticotrophs secrete and where from

A
  • ACTH

- from ant pit

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12
Q

what do gonadotrophs secrete

A
  • LH (luteinizing hormone) and FSH (follicular stimulating hormone)
  • from ant pit
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13
Q

what kind of receptor does gonadotropin-releasing hormone activate?

A

GPCR

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14
Q

what are LH and FSH made of and what is their effects

A

glycoproteins

  • LH: causes testes to produce testosterone
  • FSH: causes ovaries to produce estrogen and testosterone
  • stimulated by GnRH
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15
Q

what acts synergistically with corticotropin-releasing hormone?

A

vassopressin and angiotensin act synergistically with CRH to mediate ACTH release
- VP = positive regulator of ACTH

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16
Q

what inhibits corticotropin-releasing hormone

A

oxytocin

- negative regulator

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17
Q

in addition to the ant pit, where is corticotropin-releasing hormone secreted?

A

placenta

as a preprohoromone? has a signal peptide AND a cryptic peptide

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18
Q

what is a long lasting negative ACTH feedback

A

cortisol acts on hypothalamus or pit…

- can be fast or slow

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19
Q

what is a slow long lasting ACTH neg feedback

A

nuclear

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20
Q

what is a fast long lasting ACTH neg feedback

A

nonnuclear

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21
Q

what inhibits prolactin?

A

dopamine (aka prolactin inhibiting hormone)

- this is the main regulatory hypothalamic hormone

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22
Q

what does prolactin inhibit?

A

gonadotropin releasing hormone

  • inhibits LH and FSH
  • therefore inhibits ovulation in females and spermatogenesis in males (testosterone, estrogen, progesterone)
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23
Q

what acts as a positive regulator for prolactin?

A

suckling on breasts

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24
Q

what are thyrotrophs stimulated by?

A

thyrotropin-releasing hormone (TRH)

- hypothalamus

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25
Q

what are thyrotrophs inhibited by?

A

somatostatin
- hypothalamus

and by thyroid hormone, T3 and T4 (negative feedback loop)

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26
Q

what does the release of growth hormone stimulate

A

the production of IGF-1, the uptake of AA in tissues, lipolysis, protein synth in liver, opposes insulin’s actions

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27
Q

what is the negative feedback for GHRH

A
  • negative feedback on somatotrophs is autocrine
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28
Q

what is the release of GHRH from the hypothalamus inhibited by?

A

somatostatin

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29
Q

what hormone from the stomach has a positive effect on GH release?

A

ghrelin

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30
Q

what is the reciprocal hormone of GHRH

A

somatostatin
- decreases cAMP and therefore decreases synthesis of GH
(GHRH does the opposite)

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31
Q

what is found in the intermediate lobe

A

melanotrophs that produce the melanocyte-stimulating hormone (MSH)

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32
Q

what does ACTH do

A
  • controls steroid secretion from the adrenal cortex (mineralcorticoids, cortisol, glucocorticoids)
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33
Q

what kind of receptor does ACTH bind to in the adrenal cortex?

A

melanocortin receptor

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34
Q

what does MSH stimulate in mammals

A

MSH stimulates melanocytes to produce melanin

- deriver of tyrosine

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35
Q

what does MSH stimulate in frogs, octopus, fish

A

MSH stimulates the distribution of pigment in melanophores

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36
Q

what inhibits MSH production in the hypothalamus?

A

dopamine

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37
Q

if you do a test and there is low testosterone, LH and FSH where is the problem

A

gonadotrophin releasing hormone

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38
Q

if you do a test and there is normal LH and FSH but low testosterone what is the problem

A

problem with target gland in the testes??

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39
Q

vassopressin main function

A

osmoregulation (water balance) and pressure regulation (vassoconstriction), stress response (ACTH release)

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40
Q

oxytocin main function

A

uterine contraction and milk ejection

also mother and offspring bonding

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41
Q

what does oxytocin inhibit

A

inhibits corticotropin-releasing hormone (CRH)/ vasopressin (VP) mediated ACTH release
- helps calm

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42
Q

what kind of receptor is the oxytocin receptor

A

GPCR

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43
Q

what does and increase in IP3 and therefore intracellular Ca2+ levels do (2)

A
  1. myosin contraction in smooth muscle causing milk-release

2. NT release leading to bonding in humans and animals

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44
Q

causes of diabetes insipidus

A
  1. hypothalamic
  2. nephrogenic (mutation of VR receptor or aquaporin channels in collecting duct)
  3. Gestational (when metabolism of VP increased during pregnancy)
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45
Q

what are the direct and indirect effects of GH

A
  1. Direct: metabolism

2. Indirect: growth

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46
Q

Direct effect of GH

A

GH binds to GHR on fat cells, causes the breakdown of fats

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47
Q

Indirect effect of GH

A

GH causes liver to produce and secrete IGF-1. acts on bone/muscles etc and causes them to grow!

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48
Q

what acts as a negative feedback regulator for GH

A

increased IGF-1 concentration

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49
Q

what inhibits GH release

A

somatostatin

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50
Q

what enhances the release of GH

A

ghrelin from the stomach… binds to secretagogue receptor

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51
Q

what hormones are important for growth

A

TH
insulin
sex hormones
glucocorticoids - high concentration = reduced growth

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52
Q

what kind of receptor does GH bind to

A

cytokine receptor (tyrosine kinase separate)

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53
Q

what binds to a similar receptor as GH binds to?

A

interleukins (a cytokine)

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54
Q

what does JAK2 do in GH pathway?

A

tyrosine kinase

  • phosphorylates itself, GHR, and STAT
  • activate PI3K and MAPK pathways that lead to growth
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55
Q

what does ubiquitin do?

A

attaches to lysine in protein.

  • turns cell signaling off
  • signals for internalization and proteolysis in proteosome
56
Q

what are 3 proteins that are important in growth hormone downregulation (and what do they do?)

A
  1. ubiquitin
  2. phosphatases
  3. SOCS (suppressors of cytokine signalling)
    - SOCS have SH2 domain that bind to JAK2 and STAT proteins and target for degradation
57
Q

disease when there is too much GH after puberty

A

acromegaly

- too much GH after puberty inc. in IGF1

58
Q

causes of increased GH action

A

-enlarged pituitary from overstimulation of regulatory hormones (hypothalamic tumour)
- ectopic GH or GHRH
(acromegaly, gigantism)

59
Q

causes of decreased GH action

A 
GH resistance (reduced function of GHR, lowered GHBP) 
- insensitivity to IGF-1 
(laron's dwarfism, normal short kids)
60
Q

what growth factors use cytokine receptors

A

erythropoietin (RBC), colony stimulating factors (WB), cytokines (immune cells), transforming growth factor beta (inc FSH, inhibits cell growth)

61
Q

what kind of receptor does prolactin bind to?

A

cytokine receptor

62
Q

growth factors that use growth factor receptors (tyrosine kinase receptors)

A

IGF-1, IGF-2, insulin, epidermal growth factor, nerve growth factor, platelet-derived growth factor

63
Q

what is the MAPK pathway (and what does MAPK stand for)

A
  • phosphorylation cascade… growth factor binding protein 2 (GRB2) binds, recruits RAS (rat sarcoma… small g-prot) and activates MAPK pathway
  • mitogen-activated protein kinase
64
Q

what does PI3K, and PDK stand for (phosphorylation cascade… what does it regulate)

A
  • PI3K = phosphoinositide 3-kinase
  • PDK = PIP3-dependent kinase
  • growth factor signaling that effects glucose pathways
65
Q

what kind of domains does GRB2 have

A

SH2 (recognizes phosphorylated tyr) and SH3 (recognizes proline rich)

66
Q

what is a disease associated with too much growth FACTOR

A

CANCER

- too little GF = failure to grow, apoptosis

67
Q

what was the first oncovirus to be described

A

rous sarcoma virus

68
Q

what does the rous sarcoma virus do

A

brings in v-src (src = encodes a tyr kinase) by mimicking c-src. This src lacks regulation because it is missing sites for phosphatase inactivation
- has tyr kinase ocogene, reverse transcriptase enzyme, and integrase enzyme

69
Q

what are the effects of TH

A

regulates metabolism, cardiovascular and other hormone function

70
Q

what is the most common endocrine disease. And what is the affected rate

A

thyroid hormone diseases (1/7 - more woman affected)

71
Q

what affects the thyroid axis in NA

A 
bisphenyl A (placticizers) 
polybrominated biphenyl ethers (flame retardants)
72
Q

what kind of sacs is the thyroid made of and what are these sacs filled with

A

made of sacs called follicles that are filled with colloid

73
Q

how does TH get made and released

A
  • thyrogobulin is produced, gets secreteed into colloid
  • tyrosine residues on thyrogobulin are iodinated by thyroid peroxidase… this is TH attached to thyrogobulin
  • when stimulated by TSH the thyrogobulin attached TH all get endocytosed
  • Thyrogobulin degraded, free TH is released in blood!
74
Q

what causes goitre?

A

not enough iodide

  • TH not released no neg feedback therefore TSH keeps pumping
  • enlarged thyroid gland
  • causes goitre
75
Q

what does too much iodine cause

A

downregulation of TH

76
Q

what TH are active in the nucleus

A

T3, T4

- only the T3 where the iodine gets removed from the outer ring

77
Q

what inhibits and stimulates TSH release

A

inhibits: somatostatin (or T3, T4 neg feedback)
stimulates: thyroid releasing hormone (TRH)

78
Q

what regulates TH

A

1) circadean rhythm and cold
2) glucocorticoid
3) chronic stress
4) excess iodide
5) autoimmune antibodies against TSH receptors
6) estrogen

79
Q

**what does TSH stimulate

A

follicle growth and TH synthesis and secretion

80
Q

what is T3 and T4 BBP?

A

thyroid-binding gobulin

81
Q

what does low thyroid-binding gobulin result in?

A

hypothyroidism

82
Q

how is TH trans into the cell and then into the nucleus?

A
  • actively transported into the cell

- diffuses into nucleus

83
Q

3 different domains of nuclear receptor

A
  1. amino terminus domain
  2. DNA binding domain
  3. ligand binding domain
84
Q

function of the amino terminus domain

A
  • ligand-independent transactivation

other cofactors bind here

85
Q

function of the DNA binding domain

A
  • dimerization
86
Q

function of the ligand binding domain

A
  • hetero/homo dimerization
  • ligand dependent transactivation
  • ligand binding
  • nuclear translocation
  • association with heat shock proteins (ONLY STEROID RECEPTORS.. NOT THYROID RECEPTORS)
  • TR STAY BOUND TO DNA IN NUC
87
Q

what kind of dimer does thyroid receptor bind as

A

heterodimer

- usually TR with retinoX?

88
Q

what happens if it is a negative TRE and there is TRE + TR + TH?

A

REPRESSING

89
Q

what are the genomic effects of TH

A
  • apoptosis

- proliferation

90
Q

examples of TH apoptosis and proliferation**

A

apoptosis: increase in transcription of caspases
proliferation: increase in transcription of caspase 3 and cyclins, cyclin D moved to S-phase for DNA synthesis

91
Q

what do TRb and TRa do?

A

TRb - autoregulates (represses w/o ligand and activates itself)
TRa - upregulated by TRb and 5’ deiodinases to enhance activation

92
Q

why was this a good paper to do

A

thyroid hormones are

  1. highly conserved between species
  2. measurable endpoint
  3. affects metabolism, growth and development in vertebrates
93
Q

when there was an increase in POP what happened to the TH receptors and the TH

A

TH receptor alpha increased when more POP

TH (thyroxine) decreased with more POP

94
Q

why were harbour seals a good model for this paper

A
  1. abundant
  2. non-migratory
  3. biology and physiology well studied
  4. has been used to determine POP hotspots and as a model for the relationship between contaminants and health effeects
95
Q

what were the three sites used in the seal paper and what were they used for

A
  1. Queen Charlotte Strait
    - reference site (cleanest)
  2. Smith Island
    - medium conamination
  3. Gertrude island
    - most contamination
96
Q

what site were TR’s the highest

A

gertrude island (TRa and TRb significantly higher)

97
Q

as PCB increases what happens to TT4 and TRa?

A

as PCB concentrations in water increases TT4 decreases and TRa increases

  • R value shows how much these are correlated
  • p-value shows the level of significance (here is 0.01)
98
Q

characteristacs of POP’s

A
  • lipophilic
  • bioaccumulate
  • long half life
99
Q

what thyroid hormones promote actin polymerization in rat brain cells

A

T4, rT3

100
Q

what happens when baby has hypothyroidism

A

cretinism

101
Q

what is graves disease characterized by (triad)

A
  • goitre
  • hyperthyroidism
  • bulging eyes
102
Q

3 symptoms of Hashimoto’s disease

A
  1. weight gain
  2. lethargy
  3. menstrual irregularity
  4. depression
  5. cold intolerance
103
Q

symptoms of graves disease

A
  1. weight loss
  2. profuse sweating
  3. cardiac arrhythmeas
  4. bulging eye
104
Q

why are deiodinases so important

A
  • important for regulating metabolic processes
  • regulating TH action during development
  • and regulating feedback control of the thyroid axis
105
Q

what causes graves disease?

A

autoimmune destruction of thyroid gland

106
Q

what is on the ligand-independent transactivation domain of the nuclear receptor

A

Activation function 1 (AF-1)

  • change confirmation without ligand
  • can lead to coactivation or corepression
107
Q

what is on the DNA binding domain

A

2 zinc fingers

  • highly homologous
  • allows dimerization and binding to hormone response element
108
Q

what HRE binds as homodimers

A

invert and palendrome

- estrogen R, glucocorticoid, mineralcorticoid, progesterone, androgen (response elements)

109
Q

what binds as heterotimers

A

direct repeat

  • TRE
  • TR + retinoic X receptor (most common)
110
Q

what is typical structure for ligand binding domain

A

12 a-helices and beta turn

111
Q

what initiates mitochondria apoptosis and what does the mitochondria release

A
  • initiated by p53, releases cytochrome c

- caspase 9 then activated DNA is cut

112
Q

what does the zona reticularis produce and what is it deficient in

A

produces cortisol and androgens

- deficient in aldosterone enzymes (P450 aldosterone)

113
Q

what does the zona fasiculata produce and what is it deficient in

A

produces cortisol and androgens

- deficient in aldosterone enzymes (P450 aldosterone)

114
Q

what does zona glomerulosa produce and what is it deficient in

A

produces aldosterone

- deficient in cortisol and androgen enzymes (17-a hydroxylase)

115
Q

what is the zona glomerulosa regulated by?

A

ACTH, and the renin-angiotensin system

116
Q

what is abundant in the zona fasiculata

A

mitochondria, lipid droplet, SER

117
Q

what does aldosterone promote (produced in ZG)

A
  • Na+ retention K+ excretion
118
Q

what does glucocorticoids promote (produced in ZF, ZR)

A
  • protein and carbohydrate catabolism, gluconeogenesis,
119
Q

what are sex steroids secreted from

A

zona reticularis (estrogen, androgens converted to testosteron)

120
Q

what kind of receptors can glucocorticoids bind to?

A

glucocorticoid receptors OR mineralcorticoid receptors

121
Q

how does cortisol travel in blood

A
  • corticosteroid binding gobulin

- albumin

122
Q

what are cortisols functions

A

maintains normal glucose level in blood by:

  • stimulating gluconeogenesis in liver
  • inhibition of glucose uptake in muscle and adipose
  • fat breakdown in adipose tissue
123
Q

how do glucocorticoids reduce inflammation

A
  • decrease enzymes involved in prostaglandins

- induce apoptosis in lymphocytes (especially T cells)

124
Q

how does glucocorticoids play a role in fetal developmetn

A
  • involved in the development of many systems through the use of growth factors
  • production of surfactant
  • high levels of glucocorticoids inhibits growth in children
125
Q

what enzyme converts cholesterol to pregnenolone

A

cytochrome p450 oxidase

126
Q

how is cortisol synthesised (what receptor, what binds)

A

GPRC, ACTH binds

- when PKA activated , cholesterol is released from lipid droplet

127
Q

what are the proteins involved in changing cholesterol to pregnenolone

A
  • stAR (steroidogenic acute regulatory protein) - puts cholesterol in mitochondria
  • p450scc (modifies cholesterol side chains in mitochondria to change it to pregnenolone)
  • SER can cange pregnenolone to cortisol
128
Q

what hormone is a natural agonist, a synthetic agonist and a synthetic antagonist

A

agonist: cortisol
synthetic agonist: prednisone
synthetic antagonist: taximofen

129
Q

hormones with BBP

A
  • cortisol
  • GH
  • IGF-1
130
Q

how iron levels are controlled

A
  • anemia hypoxia in kidneys
  • erythropoeiten is released (stimulates synth of RBC)
  • as RBC increases, erythroferrone released from bone marrow
  • erythroferrone stimulates the liver to produce hepcidin
  • downregulates release of hepcidin (iron levels increase, from duodenum)
  • this increases the carrying capacity of RBC
131
Q

what does COPII do

A

mediates anterograde (COP = coat associated protein)

132
Q

what does COPI do

A

mediates retrograde

133
Q

what does clatherin do

A

mediates the transfer of vesicles from trans golgi to the membrane

134
Q

what uses growth factor receptor (tyrosine kinase)

A
  • insulin
  • IGF-1
  • epidermal growth factor

GF, GFR, SH2, SH3, MAPK3

135
Q

what kind of signaling pathway is oxytocin a part of

A

GPCR

gaq (muscle contraction for milk release)

136
Q

what activates guanylyl cyclase receptor and what does it cause

A

atrial natriuretic peptide

- causes high BP (vasodialation)

137
Q

where is iron released from

A

gut liver WBC

Biol 432 (2 decks)

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