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BIOL 3421 - molecular biochem > hormonal control of metabolism II > Flashcards

hormonal control of metabolism II Flashcards

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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
which type of adipose contains a single lipid droplet
WAT
26
what is another name for the uncoupling protein UCP1
thermogenin
27
describe what NORMALLY happens to protons after the formation of the proton gradient from the ETC
the protons would normally flow back into the matrix through ATP synthase to generate ATP
28
describe what happens to protons from the proton gradient of the ETC when thermogenin (uncoupling protein) is present
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
29
T or F: thermogenin allows lots of ATP production
false; no ATP is made, and instead the energy formed is released as heat
30
which adipokine is secreted from adipocytes in a prolonged fast
adiponectin
31
briefly, what does adiponectin do (ie which general processes does it upregulate and downregulate)
upregulates energy-producing processes and downregulates energy-consuming processes
32
specifically, which processes does adiponectin upregulate/increase
uptake of FAs from blood into myocytes, rate of b-ox in myocytes, increases appetite
33
specifically, which processes does adiponectin block/inhibit
blocks FA synthesis, cholesterol synthesis, and GNG. Inhibits thermogenesis
34
what is a myocyte
muscle cell
35
which enzyme does adiponectin stimulate
AMP-activated protein kinase (AMPK)
36
describe the energy levels that are present when AMPK is activated by adiponectin
low energy levels
37
which molecule activates AMPK during low energy levels
AMP
38
which molecule inhibits AMPK during high energy levels
ATP
39
list 6 target tissues of AMPK
heart, skeletal muscle, brain, pancreas, liver, adipose
40
list 4 target enzymes of AMPK
GLUT4, HSL, FASI, ACC
41
how does AMPK activate/inactivate target enzymes
via phosphorylation
42
AMPK role in individual cells?
monitors nutrient status and can shift metabolism towards energy generation
43
AMPK role in hypothalamus?
monitoring nutrient status across the entire organism through bottom-up pathways
44
what is ghrelin
an appetite stimulant
45
where in the body is ghrelin found
stomach
46
list 4 molecules that all affect AMPK levels in the hypothalamus
ghrelin, leptin, adiponectin, insulin
47
which pathways in the hypothalamus are initiated to adjust feeding behaviors once AMPK levels have changed
top-down hormonal pathways
48
by how many years does diabetes reduce the lifespan
5-15
49
list 3 things that a person with diabetes is more likely to be hospitalized for
cardiovascular disease, renal disease, lower limb amputation
50
which type of diabetes is more common
type 2
51
what is happening in the body during type 1 diabetes
autoimmune response: immune system destroys pancreatic B cells
52
type 1 diabetes: when does it begin
childhood
53
type 1 diabetes: treatment?
daily insulin injections, life-long management of dietary intakes and activity levels
54
type 1 diabetes: preventable?
very hard to prevent this type
55
type 1 diabetes: severity of symptoms?
quickly become severe and life threatening
56
type 2 diabetes: what's happening in the body
insulin is produced by the body develops resistance
57
type 2 diabetes: when does it start
adulthood
58
type 2 diabetes: severity of symptoms?
milder at first but organs accumulate damage over time
59
type 2 diabetes: typical weight of patients?
obese
60
what is the third type of diabetes
gestational
61
gestational diabetes occurs in _-_% of pregnant women
3-20%
62
gestational diabetes: what's happening in the body (of the mother)
hormonal changes = mom can't produce enough insulin
63
gestational diabetes: result to the mother?
increased risk of type II diabetes later in life
64
gestational diabetes: result to the fetus?
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
how was the cause of diabetes discovered in dogs
scientists removed pancreas from dogs --> they then drank lots of water, produced more urine, and urine had high glucose levels. Dogs eventually died
66
before the discovery of insulin, what was the treatment for diabetes
prolonged + severe calorie restriction to keep blood glucose levels low
67
describe the experiment that lead to insulin discovery (+ name the two scientists)
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
what does the lipid toxicity theory suggest
suggests at how obesity contributes to insulin resistance
69
lipid toxicity: describe what happens to adipocytes as an individual gains weight
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
lipid toxicity: what protein do TAG-filled adipocytes release
MCP-1
71
lipid toxicity: what does MCP-1 do
attracts macrophages to adipocytes
72
lipid toxicity: what do the macrophages do to adipocytes
they enter, trigger inflammatory response
73
lipid toxicity: after macrophages initiate the inflammatory response in adipocytes, what is released
the inflammatory cytokine TNFa
74
lipid toxicity: name the inflammatory cytokine that is released
TNFa
75
lipid toxicity: what does TNFa do
promotes the release of FFAs into the blood
76
lipid toxicity: after TNFa promotes FFA release into the blood, what occurs
FFAs travel through the blood to the muscle, where they accumulate as lipid droplets
77
lipid toxicity: what is the affect of FFAs accumulating as lipid droplets in the muslce
lipid droplets in the muscle inhibit the movement of GLUT4 to the PM --> insulin insensitivity
78
lipid toxicity: how is adiponectin synthesis affected by insulin resistance
adiponectin synthesis is reduced
79
lipid toxicity: impact of less adiponectin?
lower FA ox and higher FA synthesis
80
lipid toxicity: what type of feedback does this pathway use
positive feedback loop (bad)
81
lipid toxicity: describe how this uses a positive feedback loop
excess lipids lead to insulin resistance, insulin resistance leads you to lower adiponectin = higher FA synthesis = even more lipids

BIOL 3421 - molecular biochem (20 decks)

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