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Biol 432 > Final > Flashcards

Final Flashcards

1
Q

what are 2 ways that cortisol can act on the pit. and hypothalamus

A
  1. Fast - change of cortisol levels nonnuclear

2. Slow - change of cortisol levels nuclear

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2
Q

3 ways cortisol can be regulated

A
  1. stress
  2. circadian rhythm
  3. feedback (ACTH + cortisol)
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3
Q

how is cortisol released

A

pulsatile (combination of negative and positive control on CRH)

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4
Q

when are peak levels of CRH and ACTH

A

before awakening

- decline during the day

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5
Q

how does ACTH work

A

acts on the adrenal cortex rendering release of glucocorticoids, mineralcorticoids etc; there is a greater ACTH and glucocorticoid (cortisol rise in morning)

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6
Q

where does circadian rhythm happen

A

hypothalamus

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7
Q

what hormones (and other markers) follow a circadian rhythm

A

ACTH, cortisol, body temp, HR, work level

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8
Q

why is body temp used as a marker for circadian rhythm

A
  1. studying hypothalamus = invasive
  2. body temp is easy to measure, not invasive
  3. HR and work level are easy to measure BUT are influenced by external influences
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9
Q

what cues circadian rhythm

A
  1. light/dark
  2. stress
  3. sleep pattern
  4. feeding times
  5. physical work
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10
Q

what dysregulates circadian rhythm

A
  1. Cushing’s syndrome (high cortisol levels: stress)
  2. liver disease
  3. renal failure
  4. drug addiction
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11
Q

where does CRH (cortisol regulating hormone) come from

A

hypothalamic paraventricular nucleus (from parvocellular cells)

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12
Q

where does the circadian rhythm control of cortisol secretion derive from the connections between?

A

between the hypothalamic paraventricular nucleus and the suprachiasmatic nucleus

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13
Q

what do lesions in the suprachiasmatic nucleaus tissue cause

A

locomotor activity rhythm, damaged circadian rhythmicity

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14
Q

what is the master clock of an organism

A

suprachiasmatic nucleus

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15
Q

where does the core of the SCN receive photo input from

A

retino-hypothalamic tract

- the cells involved in SCN entrainment are different than the ones involved in vision

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16
Q

where does the SCN receive non-photo input

A
  • neuropeptide Y
  • intergeniculate leaflet
  • serotonergic projections from the median raphe nucleus
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17
Q

what part of brain are sleep schedules regulated from

A

projections from the SCN to dorsomedial hypothalamus and posterior hypothalamic area

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18
Q

how can the central clock of the SCN be reset

A

LIGHT OR DARK CYCLES

  • feeding rhythms which depend on sleep/wake activity rhythms
  • through the retino-hypothalamic tract
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19
Q

what is secreted from pineal gland

A

serotonin

- gets converted to melatonin at night

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20
Q

central output from SCN

A
  • sleep/wake cycles

- cognitive performace

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21
Q

peripheral outputs from SCN

A
  • heart
  • kidney
  • liver
  • muscle
  • body temp
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22
Q

pathway of SCN: from input to output… name tracts and structures

A

input (light) –> retino-hypothalamic tract –> SCN –> hypothalamic paraventricular nucleus –> output (thermoregulation, sleep/wake etc)

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23
Q

what causes ACTH release

A

stress (infection, depression, trauma, pain)

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24
Q

what is Cushing syndrome

A

excess cortisol - remember CRH released from hypothalamus, acts on ant. pit which releases ACTH, ACTH acts on adrenal glands producing CORTISOL

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25
Q

4 symptoms of Cushing’s syndrome

A
  1. Protein depletion (muscle wasting)
  2. Fat redistribution (increased abdominal weight)
  3. Mental problems (depression/mania)
  4. Inhibition of bone formation (impair vit. D and metabolism)
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26
Q

causes of Cushing syndrome

2 causes

A
  1. excessive endogenous production of cortisol
    - ACTH dependent
    - ACTH independent
  2. administration of glucocorticoids for therapeutic purposes
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27
Q

different kinds of excessive endogenous production of cortisol

A
  1. pituitary ACTH dependent (excessive secretion of ACTH in ant pit from tumour)
  2. ACTH-independent (tumour in adrenal cortex)
  3. ectopic ACTH (tumour)
  4. ectopic CRH(tumour)
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28
Q

note about question on final ACTH what tissue????

- don’t get it but prob memorize

A
  • muscle
  • lymphoid
  • connective
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29
Q

Addison’s disease

A

hyposecretion of glucocorticoids/mineralcorticoids from adrenal cortex
-hypoadrenocorticism (too little cortisol and aldosterone)

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30
Q

what is Addison’s cause and what does this lead to**

3

A

underproduction of cortisol from the adrenal cortex, leads to lack of NEGATIVE feedback on the pituitary… leads to an increase in ACTH secretion*

  • stimulates melanin synthesis and bronzing of skin
  • hypoglycemia
  • Na+ and K+ imbalances due to aldosterone deficiency*
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31
Q

what does cortisol do

A

control blood sugar levels, regulate metabolism, reduce inflammation

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32
Q

where in aldosterone produced

- what enzyme is expressed and what enzyme is not expressed to produce this

A

zona glomerulosa

  • p450aldo expressed
  • lacks 17a-hydroxylase so can’t produce cortisol or androgens
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33
Q

what is the physiological affects of aldosterone (a mineralcorticoid): where is main target

A
  • regulates Na+ and K+ in extracellular fluids
    MAIN TARGET: distal tubule of kidney
    1) increases active resorption of Na+
    2) increases passive resorption of water (due to Na resorption)
    3) increased renal excretion of K+
    *** these all lead to increase in BP and blood volume
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34
Q

what is the major net effect of aldosterone (how does it do this)

A

to conserve body sodium

  • activation of Na+ channel (Na reabsorbed, uptake from lumen)
  • activation of Na/K ATPase gene
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35
Q

what are regulators of aldosterone secretion

A
  1. concentration of K+ in extracellular fluid
    - increase in K+ leads to increased aldosterone secretion (replace K for Na)
  2. Angiotensin II (and ANP)
    - positive regulation: angiotensin II causes vasoconstriction increasing bp (increases aldosterone)
    - negative regulation: increase in atrial natriuretic peptide causes vasodialation decreasing bp
    - DECREASES aldosterone secretion decreasing water and Na+ to decrease bp
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36
Q

Renin-angiotensin-aldosterone axis

A
  • low BP/high K+ stimulates renin release from juxtaglomerular cells
  • renin converts angiotensinogen to angiotensin I
  • angiotensin converting enzyme (ACE) converts antiotensin I to angiotensin II
  • angiotensin II binds to angiotensin II R (increase bp: vasoconstriction, aldosterone sec, increase HR, ADH secretion - upregulation of aquaporins)
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37
Q

hyperaldosteronism

A
  • caused by adrenal tumour
  • too much cortisol and aldosterone produced
  • cushing-like symptoms
  • too little K in circulation, too high Na and water
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38
Q

what enzyme allows aldosterone and cortisol to bind to same receptor without competition - bind to mineralcorticoid receptors

A

11-b-hyroxysteroid dehydrogenase

  • cells that want aldosterone to bind express this
  • these cells convert cortisol to cortisone (biologically inactive weak affinity)
  • need this because cortisol is 100x higher in serum than aldosterone
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39
Q

what happens with chronic licorice intoxication

A

pseudohyperaldosteronism

  • no inactivation of cortisol to cortisone in kidney
  • Na and water retention, low K+. Hypertension and low renin activity (don’t know why low renin…)
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40
Q

what are the two types of cells found in the testes

A
  1. leydig cells

2. sertoli cells

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41
Q

testosterone/estradiol synthesis: what does 17a-hydroxylase convert

A

converts pregnenalone to 17a-hydroxypregnenalone

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42
Q

testosterone/estradiol synthesis: what does aromatase convert

A

converts testosterone to estradiol

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43
Q

testosterone/estradiol synthesis: what does 5a-reductase convert

A

coverts testosterone to dihydrotestosterone

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44
Q

what is the full synthetic pathway from cholesterol to estradiol/dihydrotestosterone

A

LOOK IN NOTEBOOK

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45
Q

hypothalamic pituitary gonado axis (testosterone axis)

A

GnRH (hypothalamus) –> LH (ant. pit) –> testosterone (leydig cells in testes)

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46
Q

functions of testosterone

A
  • spermatogenesis

- anabolic effects on enzymes in kidney muscle, liver

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47
Q

what do testosterone levels in blood depend on (3)

A
  1. total # of leydig cells in testes
  2. steroidogenic abilities of leydig cells
  3. LH levels (depend on GnRH)
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48
Q

how does testosterone travel through blood?

A

sex hormone binding globulin

  • this is synthesized in liver
  • free testosterone enters cell
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49
Q

leydig cell function

A
  • produces and secretes testosterone

- LH has big effect on leydig cells

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50
Q

what gives leydig cells positive/negative feedback feedback

A

negative: estradiol and testosterone
positive: FSH!! (activin)

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51
Q

leydig cell making axis

A

GnRH –> LH (ant. pit) –> increase AC, cAMP –> increase steroidergenic acute regulatory protein –> stimulates testosterone transcription and release

  • express GPCR
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52
Q

what receptor do sertoli cells have

A

FSH receptor (GPCR)

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53
Q

sertoli cell function

A

makes array of hormones (testosterone, DHT, estradiol)
- has array of enzymes to make these hormones
spermatogenesis

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54
Q

sertoli cell axis

A

FSH binds to FSH-R (GPCR) –> increase AC, cAMP –> increase androgen binding protein –> increase the [testosterone] in seminiferous tubules stimulating spermatogenesis

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55
Q

inhibin

A
  • inhibits FSH secretion from pit

- produced by sertoli cells in male

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56
Q

activin

A
  • activates FSH secretion and binding

- produces by leydig cells

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57
Q

follistatin

A

binds activin

- decreases FSH synthesis!!

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58
Q

what enzyme do granulosa cells lack

A

17a-hydroxylase (no androgens)

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59
Q

what do granulosa cells secrete

- what do they secrete in luteal phase?

A

estradiol and activin

- in luteal phase secrete projesterone and inhibin

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60
Q

what do theca cells make

A

androstenediol

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61
Q

what do theca cells lack

A

lack aromatase so can’t make estradiol

- lack FSH-R and aromatase

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62
Q

what is needed for estrogen production

A

FSH

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63
Q

what does increased E2 render in the menstrual cycle

A

increased sensitivity of pituitary to GnRH

  • initially slows it down but then it speeds up
  • speed up is what causes LH surge
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64
Q

what is ovulation (and what day is it)

A

LH surge due to increase in E2 from the FSH production ~ day 14

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65
Q

what happens after ovulation (luteal phase)

A
  • the corpus lueum favours production of progesterone
  • GnRH pulse slows
  • there is an increase in inhibin which decreases FSH
  • later, higher levels of LH increase activin; increased FSH restart the cycle
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66
Q

what causes the GnRH pulses

A

oscillation of electrical activity in the hypothalamus

- neural, hormonal, environmental inputs influence this

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67
Q

what increases GnRH pulses

A

cAMP in neurons

  • negative feedback pathways may decrease cAMP levels by inhibiting AC and activating a phosphodiesterase
  • this stimulation and inhibition regulate excitability of hypothalamic neurons: clock
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68
Q

where are 3 sites for calcium exchange in extracellular fluid

A
  1. bone
  2. kidney
  3. intestine
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69
Q

what tells kidney to release Ca

A

parathyroid gland makes parathyroid hormone which tells kidney to release Ca

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70
Q

why is calcium important

A
  1. extracellular calcium
    - excitation of heart muscles
    - synapse
  2. intracellular calcium (10,000 more outside)
    - for the use of Na+/Ca exchanger (3 na in, 1 ca out)
    - important 2nd messenger
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71
Q

what does calcitonin do

A

reduces calcium levels in the blood

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72
Q

what does parathyroid hormone do

A

increase calcium levels in blood

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73
Q

what happens if parafollicular (in thyroid gland) cells are removed

A
  • they make calcitonin

- either no calcitonin is made or there is a tumour with excess calcitonin

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74
Q

where do you find vit. D receptors

A

bone, kidney, gut (initestine) also in immune cells (testes, breast)

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75
Q

what receptors do osteoblasts have

A

receptors for vit. D and parathyroid hormone

- bone forming cell

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76
Q

what are osteoclasts inhibited by**

A

CALCITONIN

  • calcitonin reduces ca in blood
  • calcitonin stimulates Ca deposition in bone; stimulates osteoblasts
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77
Q

how long does the bone cycle take

A

6 months

  • can lose bone each time if cycle is out of balance
  • why it is detrimental to lose bone by breaks
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78
Q

what is parathyroid hormone inhibited by **

A

calcium (v sensitive)

- parathyroid cells have ca receptor (GPCR)

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79
Q

what is stimulated by increased calcium**

A

parafollicular cells (make calcitonin)

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80
Q

what hormone is critical in fish

A

calcitonin - high ca in water

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81
Q

main effect of calcitonin

A
  1. inhibits osteoclasts

2. inhibits Ca2+ absorption from gut (lowers blood ca)

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82
Q

vit. D functions

A
  1. keep Ca and phosphorus @ normal level in blood (increases ca)
  2. antiproliferation!! ~ important implications in cancer
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83
Q

what is calcitriol

A

active vit D

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84
Q

when is Vit. D secreted **

A

low Ca, low phosphorus, high PTH

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85
Q

what will happen if there is high vit. D

A
  1. inhibit its receptor transcription

2. signal hydroxylase that breaks down vit. D

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86
Q

what enzyme oxidizes the vit. D precursor… where

A

cytochrome p450 oxidase

- first acts on it in liver then transported to kidney where it is converted to active!!

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87
Q

where can excess vit. D be stored

A

liver

- vit. D precurser oxidized in liver: this is where/how it is stored

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88
Q

what does vit. D increase the transcription of (intestine)

A

Ca2+ channels, calcium binding proteins, vit. D receptors

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89
Q

what affect does vit. D have on bone

A

stimulates bone formation and Ca2+ binding, decreases PTH

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90
Q

hyperparathyroid disease

A
  • causes HYPERCALCEMIA

- too much PTH… Ca2+ does not have neg feedback

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91
Q

what is used to treat hyperparathyroid disease

A

calcitonin

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92
Q

Rickets disease (what does this cause)

A
  • lack of vit. D in children
  • causes decreased Ca and phosphorus
  • also causes rise in PTH and increased bone resorption
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93
Q

Osteomalacia Disease

A
  • mineralization of new bone is defective - adults
  • lack vit. D (low Ca or phosphate)
  • associated with osteoporosis
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94
Q

vit D deficiency (2 types)

A
  1. Type I
    - due to environment or genetic effect
  2. Type II
    - normal vit. D levels but defect in receptor
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95
Q

what is Type II vit. D deficiency called

A

alopecia

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96
Q

what is Lytic Paget’s disease (what do u treatwith)

A
  • rapid bone loss

- treat with calcitonin

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97
Q

what is Renal Secondary Hyperparathyroidism

A

kidney failure results in vit. D deficiency

- decreased Ca2+ and increased PTH!!

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98
Q

what is associated with osteoporosis

A

low estrogen and high glucocoricoids

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99
Q

osteoporosis treatment

A

calcitonin, diet, exercise

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100
Q

what affect does estrogen have on bone

A

stimulates osteoblasts and inhibits osteoclasts (stop bone breakdown)

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101
Q

what affect does testosterone have on bone

A

increased (strenthens bone growth, can be converted to estrogen)

102
Q

what affect do glucocorticoids have on bone

A

bone loss

103
Q

what cells are found in the adrenal medulla

A

chromaffin cells

104
Q

adrenal cortex layers

A

top: zona glomerulosa
middle: zona fasiculata
bottom: zona reticularis

105
Q

what does the autonomic NS consist of

A
  1. parasympathetic NS
  2. sympathetic NS
  3. enteric NS
106
Q

sympathetic NS pathway

A

brain –> pre-ganglia –> post-ganglia –> secretes norepinephrine –> innervates adrenal medulla –> AM secretes epinephrine

107
Q

where does epinephrine bind**

A

a1 or a2/b adrenergic receptor

108
Q

what type of receptor is the a1 adrenergic receptor

A

GPCR (Gaq)

109
Q

what type of receptor is the a2 adrenergic receptor

A

GPCR (Gai)

110
Q

what type of receptor is the b adrenergic receptor

A

GPCR (Gas)

111
Q

what stimulates the secretion of norepinephrine and epinephrine from the adrenal medulla (and what receptor does it use)

A

ACh

- nicotinic R

112
Q

what % is serum norepinephrine and what is it due to?

A

10-20%

- due to nerve leakage

113
Q

what is the catecholamine synthesis pathways

A

tyrosine –> (tyrosine hydroxylase) –> DOPA –> dopamine –> norepinephrine –> epinephrine

114
Q

what reaction occurs for norepinephrine to epinephrine (and what enzyme is used)

A
  • methylation (adds methyl group to norepinephrine)

- enzyme: phenylethanolamine-N-methyltransferase)

115
Q

what reaction occurs from DOPA to dopamine and what enzyme

A
  • decarboxylation

- DOPA dexarboxylase

116
Q

what hormone is stored and readily releasable in the adrenal medulla

A

epinephrine

117
Q

what is sexual differentiation driven by* *

A

presence or lack of androgens

118
Q

what does SRY do

A

protein that initiates the testes in males

119
Q

what protein initiates the wolffian ducts

A

anti-mullerian hormone

- wolffian ducts in males!

120
Q

what are the ducts that females have

A

mullerian ducts

  • form the uterus, fallopian tubes, upper part of vag
  • form from urogenital ridge
  • default if no androgen exposure
121
Q

what do wolffian ducts form

A

form epididymis, vas deferens, seminal vesicles

122
Q

what is critical for development of wolffian ducts

A

have to be exposed to testosterone before embyrogenesis and development

123
Q

what is the anti-mullerian hormone produced by

A

leydig and sertoli cells

- controls the stabilization of wolffian ducts

124
Q

what comes first: ovarian or testicular development

A

testicular

- because leydig cells form first

125
Q

what are 4 conditions associated with amenorrhea

A
  1. GnRH deficiency (Kallman’s Syndrome)
  2. Functional Hypothalamic amenorrhea
  3. Hyperprolactemia
  4. Menopause
126
Q

what is Kallman’s syndrome

A
  • no migration of GnRH producing cells or olfactory neurons to the hypothalamus
  • no sexual maturity or smell
  • GnRH deficiency
127
Q

what is functional hypothalamic amenorrhea

A
  • low pulsatile GnRH release
128
Q

what is associated with functional hypothalamic amenorrhea

A

low FSH, LH and leptin

129
Q

hyperprolactemia (why does it happen)

A

dopamine is not inhibiting prolactin release

130
Q

why does menopause happen

A

ovary stops functioning (avg. age 52)

131
Q

what are 6 examples of intersex

A
  1. kleinfelter’s syndrome
  2. turner’s syndrome
  3. male hypogonadism
  4. intersex 46 XX (female pseudohermaphroditism)
  5. intersex 46 XY (male pseudohermphroditism)
  6. androgen insensitivity syndrome (46 XY)
132
Q

kleinfelter’s syndrome: code, symptoms

A

male 47 XXY (mostly male.. depends on androgen:estrogen ratio)

  • gonadal dysgenesis
  • low testosterone and androgens
  • mental retardation: rare
  • 1/500
133
Q

turner’s syndrome: code, symptoms

A

female 45 X

  • almost no estrogen or progesterone
  • no secondary sex characteristics
  • developmental probs (hearing/kidney function)
  • fetus usually dies 1/5000
134
Q

male hypogonadism

A 
female characteristics (developmental default = female) 
- lack ability to respond to androgens
135
Q

Intersex 46 XX: appearance and causes (3)

A

female pseudohermaphroditism

  • when females with 2 X chromosomes have male phenotype appearance
    1. 21a-hydroxylase deficiency
  • makes androgens… increased testosterone and masculinization
    2. aromatase deficiency
  • lack of estrogen
    3. increased androgen exposure in utero
136
Q

what happens if there is androgen exposure @ 12 weeks

A

both penis and ovaries

137
Q

Intersex 46 XY: causes (3)

A

Male pseudohermaphroditism

  • all androgen biosynthetic dysfunctions
    1. LH receptor mutation (or SR-1 mutation)
  • decreased androgen (testosterone) production
  • hypogonadism
    2. 17a-hydroxylase deficiency
  • can’t make androgens (testosterone). have ambiguous gonads or femitization
    3. 5a-reductase deficiency
  • converts testosterone to DHT
138
Q

androgen insensitivity syndrome

A
  • testes present but absent wolffian ducts. Female appearing genetalia
  • testosterone doesn’t bind to androgen receptor as it does normally
  • androgen receptor mutation common!!
  • female secondary sex characteristics but no menarche
139
Q

what is the difference in melatonin lvls between rotating night shift workers and day shift workers

A
  1. later acrophase (peak time)
  2. lower peak amplitude
    - - these changes in melatonin lvls may be related to change in sex hormones
140
Q

what were the 2 models adjusted for

A
  1. model 1
    - smoking
    - age
    - BMI
  2. model 2
    - other sex hormones
    - menstrual phase and menopausal status
141
Q

what were results

A
  • higher estradiol and progesterone in all groups working rotating shift work
  • highest lvls of estradiol = pre-menopausal women
  • lower testosterone
  • no change in cortisol
  • rise in DHEA in women in their follicular phase!!! (other women not significant)
142
Q

why is level of DHEA important in this shift-worker paper

A

because this means more androgens that can get converted into estrogen

143
Q

where are glucagon receptors found

A
  • liver

- kidney

144
Q

where are insulin receptors found

A

everywhere

145
Q

what do delta cells in pancreas secrete

A

somatostatin

146
Q

what cells does insulin activate/inhibit

A

activates b-cells and inhibits a-cells

147
Q

what cells does glucagon activate/inhibit

A

activate all (b, a, d cells)

148
Q

what does b-cells secrete

A

insulin

149
Q

what are proteins that amplify insulin’s effects called (and where are they released from)

A

incretins

- released from small intestine

150
Q

2 incretins that are released from the small intestine

A
  • incretins amplify insulins effects!!
    1. Glucagon-like peptide 1 (GLP-1)
    2. Gastric Inhibitory Peptide
151
Q

what does glucagon-like peptide 1 do

A
  • acts on the pancreas: stimulates insulin transcription and release
  • decreases secretion of glucagon
  • slows gut emptying; increasing absorption
152
Q

what do we use to make insulin

A

recombinant DNA technology (genetic recombination)

153
Q

how is insulin synthesis regulated

A

stimulated by insulin at RECEPTOR TYROSINE KINASE

- GLUCOSE SENSOR

154
Q

how is insulin secreted

A
  • insulin takes oven 1 hr to make so it is stored
  • secretion stimulated by glucagon-like peptide 1 acting on GPCR
  • also influx of Ca
155
Q

what are 3 hormones that use receptor tyrosine kinase

A
  1. IGF-1 (insulin-like growth factor 1)
    - negative feedback on GH
  2. IGF-2 (insulin-like growth factor 2)
    - fetal growth
  3. insulin
156
Q

How does the insulin receptor tyrosine kinase function?

A
  1. signal complex (add phosphate to substrates that recruit proteins)
  2. phosphorylation cascades
157
Q

how does evolution occur

A

gene duplication (split a gene and change it without mutation occurring)

158
Q

insulin effects (5)

A
  1. metabolic
  2. cell growth
  3. fetal growth
  4. suppresses glucagon transcription
  5. brain function
159
Q

what are the 2 pathways of insulin signaling

A
  1. mitogenic (growth via MAPK)
  2. metabolic (after a meal via PI3K/PKB)
    - sometimes cell will do both
160
Q

what do SH2 domains recognize

A

phosphorylated tyrosines

161
Q

what do SH3 domains recognize

A

proline rich sequences

162
Q

what binds to the tyrosine kinase receptor and acts as a dock for other proteins

A

IRS - insulin receptor substrate

163
Q

what degrades insulin receptors (downregulated)

A

gets internalized, insulinases degrade

164
Q

what is leprechaunism

A
  • defective insulin receptor
  • some mutations lead to less severe phenotype: insulin resistance
  • heterozygous mutations v. severe (elf)
  • heterozygous: free of disease but some ppl w leprechaunsim will carry another mutation of insulin gene and show symptoms
165
Q

difference in symptoms between type 1 and 2 diabetes

A

1: weight loss, never asymptomatic

2. no weight loss (obese), often asymptomatic

166
Q

what are 3 requirements for type 1 diabetes *

A

1) b-cell reactive T-cells must be activated
2) the responses need to be proinflammatory
3) the regulation of autoreactive responses must fail

167
Q

type 2 cases - 2 cases with extreme insulin resistance

A
  1. leprechaunism (receptor defected)

2. when there is an antibody against a receptor

168
Q

type 2 diabetes is due to

A

hyperinsulinism

  • receptor insenstive because of this
  • signal pathway is defective
169
Q

what replaces the b-cells in type 2 diabetes

A

amylase deposits

170
Q

what are 4 treatments for type 2 diabetes

A
  1. diet/exercise
  2. drugs that lower glucose production in liver
  3. drugs that stimulate insulin secretion (hypoglycemia major side effect)
  4. drugs that affect glucose absorption in small intestine (glucagon-like peptide 1) … (increase insulin synth and secretion, dec glucagon sec)
171
Q

what is lipogenesis

A

when u eat sugar store fat

- can get sugar tolerance on high fat low carb diet

172
Q

what happens to GLUT1 with hyper and hypoglycemic

A
  • hypoglycemic: upregulation of GLUT1 so brain gets the glucose it needs
  • hyperglycemic: downregulation of GLUT1
173
Q

what is in the humoral immune system

A

mediated by b-cells (produce antibodies against a specific antigen)
- antigens that are freely circulating or OUTSIDE infected cells

174
Q

what is the cellular immune system

A

mediated by T cells

  • INSIDE infected cells
  • contains antigen presenting cells
175
Q

what do antigen presenting cells do and what do they express

A

break down proteins on the antigen presented to it
- the molecules on the antigen presenting cells that present the antigen are called “major histocompatibility complexes (MHC)”

176
Q

where are T cells produced

A

thymus

177
Q

what are the 2 different types of T cells (and what do they do)

A
  1. cytotoxic T cells
    - kill infected cells
  2. helper T cells
    - help other cells in the immune system
178
Q

where are potentially dangerous T and B cells eliminated

A

thymus and bone marrow

179
Q

where are MHC class II and I receptors found

A
  • MHC class II receptors found on antigen presenting cells

- MHC class I found on all other cells

180
Q

what are the 4 steps for antigen recognition by T cells

A
  1. Antigen uptake (APC)
  2. Antigen presentation
  3. T cell activation
  4. T cell inactivation
181
Q

what happens in step 3: T cell activation

A

second signal provided by CD80/86-CD28 (CD28 is on T cells)

  • this induces the expression of CD 154 and later CD152
  • CD154 binds to CD40 on APC
  • these APC-T cell interaction causes the proliferation of downstream T cells
182
Q

what happens in step 4: T cell inactivation

A
  • CD152 (expressed 48-72 hours after T cell activation) will bind to CD80/86 on antigen presenting cells because of its higher affinity
  • this replaces CD28 and initiates T cell activity/death
183
Q

SUMMARY: what 2 signals are required for (both TH and TC cells to activate)

A
  1. the TCR expressed antigen specific receptor binds to the MHC compex
  2. CD28 (on T cell) binds to CD80/86 on APC: leads to T cell proliferation
184
Q

autoimmunity is ________

A

multifactorial

185
Q

what are 5 possible disruptors of self tolerance (5)** multifactorial

A
  1. defects in apoptosis-related molecules
  2. defects of CD152 on T cells may prevent apoptosis of autoreactive T cells
  3. defects in B cell tolerance
  4. defects of regulatory T cells ***
  5. hypocortisolism (may underlie pathology behind inflammation, pain, fatigue)
    - both environmental and genetic factors involved
186
Q

Central T cell tolerance in the thymus (5 steps)

A
  1. pre T cells rearrange their T cell receptor
  2. unproductive (non functional) rearrangements lead to apoptosis
  3. productive (functional) are then tested for antigen recognition
  4. apoptosis for cells based on their ‘too high’ or ‘no avidity’
  5. surviving low-avidity cells reach periphery of CD4 or CD8 cells
187
Q

what are three environmental factors involved in autoimmune disease

A
  1. toxins
  2. diet
  3. infectious agents
188
Q

what virus are babies that develop type 1 diabetes commonly exposed to?

A

Rubella virus (toxin)

  • b-cell proteins share a similar molecular structure as proteins in the rubella virus
  • b-cells become attacked
189
Q

what does 21a-hydroxylase do

A

involved with the biosythesis of steroid hormone aldosterone and cortisol

190
Q

what is associated with Addison’s disease

A

21a-hydroxylase (a cytochrome p450 enzyme involved with the production of cortisol and aldosterone)
- Addison’s: hypocortisolism

191
Q

circadian rhythm and T cells

A
  • cortisol controls # of T cells by inducing their apoptosis
  • negative cross correlations between cortisol levels and lymphosubtypes
  • CIRCADIAN RHYTHM OF CORTISOL LOWERS T CELLS
192
Q

what nerve sends signals from liver to the brain

A

vagus nerve to the nucleus tract of solaris

193
Q

what do visceral adipose cells produce a significant amount of

A

proinflammatory cytokines

- disrupt normal insulin action leading to insulin resistance

194
Q

what area of brain do adiposity signals reach and how

A

reach arcuate nucleus which go to hypothalamus

- through circulation!!

195
Q

where does the hypothalamus receive signals from

A

nucleus tract of solaris and arcuate nucleus

- hypothalamus receives orexigenic nt and anorexigenic nt

196
Q

2 orexigenic nt

A

NPY and agouti related peptide neurons

197
Q

2 anorexigenic nt

A
  • POMC and CART (cocaine-and amphetamine related transcript)
  • inhibit appetite by CCK
198
Q

what are 3 satiety signals from the GI tract

A
  1. PYY
  2. Glucagon-like peptide-1 (GLP-1)
  3. cholecytokinin
199
Q

what is PYY secreted by

A

L cells (decrease food intake)

200
Q

what is the agonist to GLP-1

A

extendin 4 (decrease food intake)

201
Q

what does leptin do

A
  • decreases food intake and increases metabolic rate
  • inhibits NPY and AgRP neurons
  • stimulates POMC and CART neurons
202
Q

what hormone is produced in adipose tissue

A

leptin

- not satiating signal; an adiposity signal

203
Q

where is the leptin receptor found (and what kind of receptor is it)

A

arcuate nucleus

- cytokine-R, signals through STAT3

204
Q

what happens to mouse with a mutation in the production of leptin or leptin receptor

A

causes obesity

205
Q

what does ghrelin do

A

stimulates hunger (adiposity signal)

206
Q

what neurons does ghrelin stimulate

A
  • stimulate NPY, and AgRP

- inhibits POMC

207
Q

what hormone does ghrelin stimulate the release of

A

growth hormone

208
Q

what glands produce ghrelin

A

oxyntic glands of stomach

209
Q

what receptor does ghrelin bind to

A

Growth hormone secretagogue receptor

210
Q

what are 6 cytokines that are produced by adipose tissue

A
  1. leptin
  2. adiponectin
  3. adipocytokines
  4. resistin
  5. estradiol
  6. angiotensinogen
211
Q

what does leptin do (in addition to appetite regulation)

A

DECREASES INSULIN SENSITIVITY. decrease insulin secretion

  • decreases intracellular lipid in muscle
  • regulation of bone absorption… heavvier = increased risk of osteoporosis
212
Q

what does adiponectin do

A

INCREASE INSULIN SENSITIVITY

  • anti inflammatory
  • inverse correlations to BMI
213
Q

what does adipocytokines do

A

DECREASE INSULIN SENSITIVITY.

PROINFLAMMATORY

214
Q

what does resistin do

A

decreases insulin sensitivity

215
Q

what does angiotensinogen do

A

regulates BP and fluid balance

216
Q

factors affecting weight gain

A

1) behaviou (diet/exercise)
2) genetics
3) age

217
Q

what hormones act on the vagus nerve

A

cholecytokine, GLP-1, PYY

218
Q

2 pathways for light

A
  1. retinohypothalamic path - circadian rhythm and endocrine functions
  2. primary optic tract - visual perception and responses
219
Q

what protein does light signal through

A

melanopsin

220
Q

what cells receive light

A

retinal ganglion cells

221
Q

health problems associated with circadian clock dysregulation

A
  1. cancer
  2. obesity
  3. insomnia
222
Q

what are hormones relating to breast cancer and the hypothamus’ exposure to light

A
  1. serotonin
  2. melatonin
  3. vitamin D
  4. GnRH
  5. estrogen
  6. progesterone
223
Q

what is exposure to night at light associated with

A

breast and prostate cancer

224
Q

what is melatonin a regulator of

A

ERa (estrogen receptor alpha)

- clear relationship to breast cancer

225
Q

what is the rate limiting step of serotonin synthesis

A

serotonin –> acetylserotonin

226
Q

what does serotonin and melatonin start out as in their synthetic pathway

A

tryptophan

227
Q

what does melatonin do to the estrogen response pathway

A

inhibits it by binding to the MT-1-R

228
Q

where is serotonin synthesized

A

in gut. rest is made in CNS

- highest serotonin levels in mid afternoon

229
Q

what does vit. D have important implications for

A

CANCER (antiproliferation)

230
Q

what does vit. D do (antiproliferation role) **

A
  • inhibits COX2 - cyclooxygenase 2 (important for prostaglandin synth)
  • inhibits estrogen receptor alpha… thus diminishing signal for proliferation
  • decreases the expression of aromatase (less estrogen)
  • induces expression of apoptotic cell death proteins (Bax and Bak) and cell cycle arrest proteins
231
Q

when does vit. D peak and where is it produced

A

after mid-day

- produced in liver

232
Q

what disorder do 25% of people with breast cancer have

A

seasonal affective disorder (SAD)

233
Q

what gene does vit. D activate the transcription of?

A
  • the initial serotonin synthesizing gene

- tryptophan hydroxylase

234
Q

what 2 hormones downregulate estrogen signaling

A

melatonin and vit. D!!

235
Q

2 hormones that decrease occur with age

A

low dehydroepiandosterone (DHEA) and testosterone

236
Q

is replacement testosterone safe? why or why not

A

no

  • increased blood clots
  • increased risk of heart attack
  • stroke
  • heart-rhythm irregularities
237
Q

what are the functions of estrogen and progesterone

A
  • maintain reproductive function

- anti-absorptive effects on bone

238
Q

what happens after menopause

A
  • risk for osteoporosis
  • risk for coronary heart disease
  • stroke and dementia

– is this related to E and P??? that decrease with age

239
Q

what happened in the estrogen replacement studies

A
  • reduced coronary heart disease by 50%
  • reduced osteoporosis
  • but increased in stroke slightly…. therefore they stopped
240
Q

what happened in the estrogen/progesterone replacement studies?

A
  • saw increase in breast cancer
  • saw increase in coronary heart disease and stroke
  • reduction in colon cancers and fractures but risk outweighed the benefits… eventually stopped
241
Q

what demographic are estrogen replacement therapies beneficial

A

women with a hysterectomy, taking E a few years close to menopause… safe and may reduce breast cancer relief.

242
Q

what wavelength of light is needed to make serotonin and vit. D

A

serotonin = 480 nm

vit. D = 295 nm

243
Q

where is ERa expressed

A

reproductive tissues and mediates majority of sexually dimorphic and reproductive functions

244
Q

where is ERb expressed

A

diverse patterns of expression: expression in prostate, brain and immune

245
Q

what is the function of the C domain on the estrogen receptor

A

DNA binding, dimerization

246
Q

what is the function of the E domain on the estrogen receptor

A

ligand binding, dimerization

247
Q

what is tamoxifen

A

ANTAGONIST of the estrogen receptor in breast tissue

248
Q

what happens in the classical nuclear action (nuclear initiated steroid signaling)

A

activation of target gene by E2/ER OR no action by antagonist tamoxifen/ER

249
Q

what happens in non-classical nuclear action (non-genomic)

A
  • mediated through GPCR
  • phosphorylated estrogen receptor is v active
  • ER regulates the transcription of genes without a HRE
250
Q

what is E2 signaling via

A

GPCR30

Biol 432 (2 decks)

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