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Endo: Sem 2 > Beyond the Classic Endocrine Glands > Flashcards

Beyond the Classic Endocrine Glands Flashcards

1
Q

how do adipocytes store energy?

A

as triglycerides and release energy and free fatty acids

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2
Q

what are two key enzymes?

A

lipoprotein lipase and hormone sensitive lipase

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3
Q

what is lipoprotein lipase?

A

found on outside of fat cells, stimulated by insulin leading to uptake of fatty acids in the circulation for storage

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4
Q

which form do circulating lipids take?

A

FFA bound to serum proteins, but mostly part of lipoproteins.

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5
Q

what are other sources of TAGs?

A

chylomicrons containing newly digested ones or VLDLs from the liver

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6
Q

what does LPL do?

A

hydrolyse TAG into FFA and glycerol, taken up and resynthesised into TAG and stored

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7
Q

what are TAGs?

A

triacylglycerides

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8
Q

what happens when there is too much glucose?

A

when theres more than can be put into glycogenesis, glucose is taken up by adipocytes and synthesised into glycerol or acetyl CoA –> TAG

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9
Q

how is energy released from TAG?

A

hydrolysis into FFA and Glycerol released into circulation via hormone senstive lipase enzyme

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10
Q

why is it called hormone sensitive lipase?

A

activity is stimulated by hormones such as adrenaline and cortisol

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11
Q

why is the energy storage more of a problem?

A

this is associated with the obesity epidemic

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12
Q

what hormones are released by the adipose tissue?

A
  • leptin
  • adiponectin
  • resistin
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13
Q

what do the hormones released by adipose tissue do?

A

act as distant targets so are therefore hormones

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14
Q

What is leptin?

A

hormone released by fat cells acting on hypothalamus receptors to trigger pathways associated with satiety. Causes response that we dont need more fat and can instead burn energy = -ve feedback

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15
Q

why is the leptin response negative feedback?

A

the leptin triggers a turn down in lipogenesis and turn down in appetite behaviour

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16
Q

why does leptin not work in obese people for weight loss?

A

obesity is more a problem with leptin resistance and high leptin rather than mutated leptin

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17
Q

what do weak androgens released by adrenal gland do?

A

convert into strong androgens and also convert androgens into oestrogens

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18
Q

what type of signalling molecule are cytokines?

A

paracrine but some can enter into circulation

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19
Q

what other hormones are released from adipose tissue?

A

adiponectin and resistin

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20
Q

what does adiponectin do?

A

potentiates insulin to maintain and increase sensitivity. in obesity, adiponectin levels decrease which compromises effectiveness of insulin

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21
Q

what is resistin associated with?

A

insulin resistance, high in obesity

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22
Q

what happens where obesity is associated with insulin resistance?

A

likely raised insulin levels –> chronic hyperinsulinaemia

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23
Q

what can insulin stimulate release of?

A

IGF-1

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24
Q

what do adipocytes do in obesity?

A

release more pro-inflammatory cytokines

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25
Q

normal fat cell?

A

high adiponectin, low leptin

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26
Q

obese fat cell?

A

low adiponectin, high leptin resistance, high resistin and more immune cells due to chemokines secreted by fat cells bringing in more macrophages.

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27
Q

implication of more adipose tissue

A

more macrophages so adipose tissue is in a semi-inflammatory state

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28
Q

why is there insulin resistance in obese individuals?

A

lots of leptin release but lots of leptin resistance, adiponectin levels decrease contributing to insulin resistance and while resistin increases, it also contributes to insulin resistance.

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29
Q

what is metabolic syndrome?

A

disorder of energy metabolism

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30
Q

what is metabolic syndrome associated with?

A
  • obesity
  • hypertension
  • raised serum glucose
  • high serum triglycerides
  • insulin resistance
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31
Q

which type of fat is worse?

A

visceral rather than subcutaneous

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32
Q

what is ghrelin?

A

hormone released from stomach, promotes feeding

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33
Q

where is leptin released?

A

adipocytes

34
Q

where do vagal afferents travel?

A

nucleas tractus solitarius

35
Q

what do leptin and vagal afferents signal to hypothalamus?

A

satiety so that hypothalamus integrates and moves towards burning fat/conserving

36
Q

what increases during absorptive phase?

A

leptin, insulin, PPY, CCK, GLP-1

37
Q

what do leptin, insulin, PPY, CCK, GLP-1 do>

A

stimulate neurones in hypothalamus leading to anorexigenic effect to inhibit food intake

38
Q

what does ghrelin do?

A

stimulates various neural pathways in hypothalamus leading to orexigenic effect to stimulate food intake

39
Q

anorexigenic effect?

A

inhibits food intake

40
Q

orexigenic effect?

A

stimualtes food intake

41
Q

what does reducing leptin do?

A

increases appetite

42
Q

what is ghrelin good at?

A

appetite stimulation

43
Q

what does mutation in LEP (leptin) gene, adipose tissue or LEPR (leptin receptor) lead to?

A

abnormal eating behaviour and early onset morbid obesity

44
Q

how can leptin deficiency be treated?

A

with leptin to result in reduced fat mass

45
Q

why is leptin treatment rarely effective?

A

single mutations are rare, its usually much more complex

46
Q

what is obesity associated with?

A

leptin resistance

47
Q

what is renin?

A

enzyme produced by kidney which can cleave pro-hormones in the circulation

48
Q

what hormone can heart cells release?

A

atrial natruiuretic peptide (ANP)

49
Q

when is ANP released?

A

in response to atrial stretch

50
Q

when does atrial stretch occur?

A

raised BP due to raised blood volume = greater venous return = greater stretching

51
Q

what are the aims of ANP?

A

to oppose/inhibit the RAAS system

52
Q

what are the effects of ANP?

A
  • vasodilation to reduce BP
  • inhibits Na+ absorption is kidney promoting diuresis
  • modulates the RAAS system by inhibiting renin so less Ang II and aldosterone which would usually increased blood volume and BP
53
Q

what does renin do?

A

converts Angiotensinogen to Angiotensin I so that Ang I –> Ang II via ACE

54
Q

when is renin produced?

A

in response to low perfusion pressure, reduced Na+ or sympathetic stimulation

55
Q

what does angiotensin II do?

A

lowers BP via vasoconstriction and stimulating adrenal cortex to secrete aldosterone

56
Q

how does aldosterone work?

A

increases salt and water retention in kidneys increasing blood volume and blood pressure

57
Q

what is erythropoietin?

A

hormone release by kidney in response to low partial pressure of oxygen in circulation

58
Q

what does erythropoitein do?

A

stimulates bone marrow to produce more RBC

59
Q

what is recombinant EPO?

A

used to treat anemia due to renal failure

60
Q

what is calcitriol?

A

hormone that synthesises active Vitamin D. Conversion into calcitriol by an enzyme happens in kidney

61
Q

what is the function of vitamin d?

A

calcium homeostasis, if calcium levels drop, activity of enzyme increases and more vitamin D released

62
Q

what are the effects of vitamin d?

A

increase absorption of Ca2+ from the gut and releases Ca2+ from bone raising Ca2+ levels.

63
Q

parathyroid hormone

A

also involved in calcium homeostasis

64
Q

what is main store of calcium?

A

bone

65
Q

what do osteocytes produced?

A

fibroblast growth factor 21 (FG23) which decreases absorption of phosphate and synthesis of active vitamin D when it reaches kidney

66
Q

what do osteoblasts produce?

A

uncarboxylated osteocalcin (uOCN)

67
Q

what does uOCN do?

A

increases insulin production and secretion in pancreatic beta cells increasing adiponectin secretion (potentiates insulin in adipocytes) and increases insulin sensitivity and glucose uptake in muscle

68
Q

examples of tumours that increase secretion of hormone?

A

pituitary adenoma, increased corticotrophs = cushing disease

69
Q

tumours can be ectopic source of hormone

A

e.g. lung tumours secrete ACTH and stimulate cortisol secretion outside of normal gland release.

70
Q

what tumours are hormone dependent?

A

breast and prostate cancer

71
Q

what do hormone dependent tumours do?

A

convert circulating precursors into biologically active steroids that stimulate their own growth

72
Q

breast tumours convert weak androgens to oestrogen

A

allows tumour to keep growing

73
Q

what is oestradiol?

A

active end product, used to therapeutically target enzymes to stop production of hormones to stop growth

74
Q

what is circadian rhythm controlled by?

A

melatonin secreted from pineal gland?

75
Q

what are circadian rhythms?

A

bodys biological clock

76
Q

how are circadian rhythms secreted?

A

in a rhythmic pattern, low in the day, rise at night

77
Q

what does circadian rhythm correlate with?

A

physiological functions e.g. body temp drop during sleep and decrease in alertness at night

78
Q

why are circadian rhythms endogenous?

A

not entrained to light-dark cycle instead they run on 24 hour cycle

79
Q

how can circadian rhythms be influenced?

A

via sensory input from environmental cues

80
Q

what controls circadian rhythm and has neural links to pineal gland?

A

suprachiasmatic nucleus

Endo: Sem 2 (11 decks)

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