hormonal control of metabolism II Flashcards

1
Q

why is hormonal control of metabolism needed?

A

needed to keep fuel intake and energy expenditure in balance so an appropriate amount of adipose tissue in maintained

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2
Q

what happens when hormonal signals that control metabolism fail + you eat/drink more calories than you need? (2)

A

you convert the excess fuel into TAGs and store them in adipocytes, and you divert the excess fuel to heat production

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3
Q

which class of hormones are released from adipose tissue

A

adipokines

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4
Q

what type of hormones are adipokines

A

peptide hormones

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5
Q

role of adipokines?

A

they inform other tissues of the adequacy of TAG energy reserved to balance fat synthesis and oxidation

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6
Q

what was the first adipokine discovered

A

leptin

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7
Q

where in the body is leptin located

A

adipose tissue (bc it’s an adipokine)

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8
Q

when is leptin secreted from adipose

A

when TAG stores are sufficient to curtail appetite and increase energy expenditure (you have enough TAGs = stop eating)

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9
Q

list 3 things that may occur in the leptin knockout method (this was done in mice experiments)

A

high cortisol, unrestrained appetite, can’t stay warm

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10
Q

where does leptin secreted from adipocytes go

A

goes into the blood and to the hypothalamus

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11
Q

what happens when leptin reaches the hypothalamus

A

hypothalamus has leptin receptors, and it activates a neuronal response that returns back to adipocytes

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12
Q

after leptin binds to the hypothalamus and it sends it’s signal back to adipocytes, which neurotransmitter do the adipocytes release

A

norepinephrine

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13
Q

what happens once adipocytes secrete norepinephrine

A

norepinephrine activates a GPCR pathway to adenylyl cyclase, which increases cAMP levels and activates PKA

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14
Q

after norepinephrine release has led to PKA activation, what does PKA do (2)

A

activates mobilization of lipid droplets + activates the expression of the uncoupling protein (UCP1) in brown adipose tissue

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15
Q

expression of which uncoupling protein is activated by PKA

A

UCP1

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16
Q

where is UCP1 activated

A

brown adipose tissue

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17
Q

purpose of BAT

A

common in newborns/hibernating animals to keep vital organs warm

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18
Q

T or F: there is much less BAT in adults

A

true

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19
Q

how can BAT synthesis be activated in adults

A

via significant cold exposure

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20
Q

describe the structure of WAT (composition + shape)

A

contains one large lipid droplet, spherical

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21
Q

describe the structure of BAT (composition + shape)

A

smaller, contains multiple lipid droplets, polygonal, contain many more mitochondria, surrounded by a denser capillary network

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22
Q

which type of adipose is spherical

A

WAT

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23
Q

which type of adipose is polygonal

A

BAT

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24
Q

which type of adipose contains multiple lipid droplets

A

BAT

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25
Q

which type of adipose contains a single lipid droplet

A

WAT

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26
Q

what is another name for the uncoupling protein UCP1

A

thermogenin

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27
Q

describe what NORMALLY happens to protons after the formation of the proton gradient from the ETC

A

the protons would normally flow back into the matrix through ATP synthase to generate ATP

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28
Q

describe what happens to protons from the proton gradient of the ETC when thermogenin (uncoupling protein) is present

A

thermogenin forms a channel in the IMM to allow protons to flow back in WITHOUT generating ATP. Allows dissipation of the H+ gradient without building ATP = energy released as heat

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29
Q

T or F: thermogenin allows lots of ATP production

A

false; no ATP is made, and instead the energy formed is released as heat

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30
Q

which adipokine is secreted from adipocytes in a prolonged fast

A

adiponectin

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31
Q

briefly, what does adiponectin do (ie which general processes does it upregulate and downregulate)

A

upregulates energy-producing processes and downregulates energy-consuming processes

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32
Q

specifically, which processes does adiponectin upregulate/increase

A

uptake of FAs from blood into myocytes, rate of b-ox in myocytes, increases appetite

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33
Q

specifically, which processes does adiponectin block/inhibit

A

blocks FA synthesis, cholesterol synthesis, and GNG. Inhibits thermogenesis

34
Q

what is a myocyte

A

muscle cell

35
Q

which enzyme does adiponectin stimulate

A

AMP-activated protein kinase (AMPK)

36
Q

describe the energy levels that are present when AMPK is activated by adiponectin

A

low energy levels

37
Q

which molecule activates AMPK during low energy levels

A

AMP

38
Q

which molecule inhibits AMPK during high energy levels

A

ATP

39
Q

list 6 target tissues of AMPK

A

heart, skeletal muscle, brain, pancreas, liver, adipose

40
Q

list 4 target enzymes of AMPK

A

GLUT4, HSL, FASI, ACC

41
Q

how does AMPK activate/inactivate target enzymes

A

via phosphorylation

42
Q

AMPK role in individual cells?

A

monitors nutrient status and can shift metabolism towards energy generation

43
Q

AMPK role in hypothalamus?

A

monitoring nutrient status across the entire organism through bottom-up pathways

44
Q

what is ghrelin

A

an appetite stimulant

45
Q

where in the body is ghrelin found

A

stomach

46
Q

list 4 molecules that all affect AMPK levels in the hypothalamus

A

ghrelin, leptin, adiponectin, insulin

47
Q

which pathways in the hypothalamus are initiated to adjust feeding behaviors once AMPK levels have changed

A

top-down hormonal pathways

48
Q

by how many years does diabetes reduce the lifespan

A

5-15

49
Q

list 3 things that a person with diabetes is more likely to be hospitalized for

A

cardiovascular disease, renal disease, lower limb amputation

50
Q

which type of diabetes is more common

A

type 2

51
Q

what is happening in the body during type 1 diabetes

A

autoimmune response: immune system destroys pancreatic B cells

52
Q

type 1 diabetes: when does it begin

A

childhood

53
Q

type 1 diabetes: treatment?

A

daily insulin injections, life-long management of dietary intakes and activity levels

54
Q

type 1 diabetes: preventable?

A

very hard to prevent this type

55
Q

type 1 diabetes: severity of symptoms?

A

quickly become severe and life threatening

56
Q

type 2 diabetes: what’s happening in the body

A

insulin is produced by the body develops resistance

57
Q

type 2 diabetes: when does it start

A

adulthood

58
Q

type 2 diabetes: severity of symptoms?

A

milder at first but organs accumulate damage over time

59
Q

type 2 diabetes: typical weight of patients?

A

obese

60
Q

what is the third type of diabetes

A

gestational

61
Q

gestational diabetes occurs in -% of pregnant women

A

3-20%

62
Q

gestational diabetes: what’s happening in the body (of the mother)

A

hormonal changes = mom can’t produce enough insulin

63
Q

gestational diabetes: result to the mother?

A

increased risk of type II diabetes later in life

64
Q

gestational diabetes: result to the fetus?

A

can cause still births, pre-term labour, larger babies (= increased likelihood of birth injuries). Large babies = at higher risk of respiratory distress, obesity, and type 2 diabetes

65
Q

how was the cause of diabetes discovered in dogs

A

scientists removed pancreas from dogs –> they then drank lots of water, produced more urine, and urine had high glucose levels. Dogs eventually died

66
Q

before the discovery of insulin, what was the treatment for diabetes

A

prolonged + severe calorie restriction to keep blood glucose levels low

67
Q

describe the experiment that lead to insulin discovery (+ name the two scientists)

A

Banting and MacLeod purified a pancreas extract from B cells (was first tested on dogs, then humans). Human version was more purified. Extract = named insulin

68
Q

what does the lipid toxicity theory suggest

A

suggests at how obesity contributes to insulin resistance

69
Q

lipid toxicity: describe what happens to adipocytes as an individual gains weight

A

adipocytes become larger as more TAGs are stored there. Eventually the adipocytes are completely filled with TAGs and can no longer accept any more

70
Q

lipid toxicity: what protein do TAG-filled adipocytes release

A

MCP-1

71
Q

lipid toxicity: what does MCP-1 do

A

attracts macrophages to adipocytes

72
Q

lipid toxicity: what do the macrophages do to adipocytes

A

they enter, trigger inflammatory response

73
Q

lipid toxicity: after macrophages initiate the inflammatory response in adipocytes, what is released

A

the inflammatory cytokine TNFa

74
Q

lipid toxicity: name the inflammatory cytokine that is released

A

TNFa

75
Q

lipid toxicity: what does TNFa do

A

promotes the release of FFAs into the blood

76
Q

lipid toxicity: after TNFa promotes FFA release into the blood, what occurs

A

FFAs travel through the blood to the muscle, where they accumulate as lipid droplets

77
Q

lipid toxicity: what is the affect of FFAs accumulating as lipid droplets in the muslce

A

lipid droplets in the muscle inhibit the movement of GLUT4 to the PM –> insulin insensitivity

78
Q

lipid toxicity: how is adiponectin synthesis affected by insulin resistance

A

adiponectin synthesis is reduced

79
Q

lipid toxicity: impact of less adiponectin?

A

lower FA ox and higher FA synthesis

80
Q

lipid toxicity: what type of feedback does this pathway use

A

positive feedback loop (bad)

81
Q

lipid toxicity: describe how this uses a positive feedback loop

A

excess lipids lead to insulin resistance, insulin resistance leads you to lower adiponectin = higher FA synthesis = even more lipids