Lecture 33: Integration of Metabolism Flashcards

1
Q

Primary fuel of the liver is

A

Fatty acids

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2
Q

Reaction rate of glucokinase and what is synthesized during fed vs starved state in liver

A

Fed- High glucokinase RR, synthesis of fatty acids/TAGS

Starve- Low glucokinase RR, synthesis of ketone bodies

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3
Q

The liver can ____ but not ___ ketone bodies

A

Can produce but not use ketone bodies

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4
Q

Which organs contain urea cycle enzymes

A

Liver/kidney

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5
Q

A decrease in NAD levels will cause what in the liver

A

Decreased: Gluconeogenesis, glycolysis, TCA cycle, B-oxidation
Increased: Lactate/ketone bodies (acidosis), TAGs

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6
Q

Which pathways will be used in the liver during fed state

A

Glycogenesis

FA synthesis

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7
Q

Which pathways will be used in fasting state in liver

A

B-oxidation of fatty acids

Glycogenolysis

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8
Q

Which pathways will be used in starved state in liver

A

B-oxidation/ketogenesis of fatty acid to form ketone bodies

Gluconeogenesis to form glucose from AAs

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9
Q

Which pathways are used during fed state in muscle

A

Glycolysis

Glycogenesis

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10
Q

Which pathways used during fasting state in muscle

A

B-oxidation/ketogenesis of FA to form ketone bodies

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11
Q

Which pathways used during starved state in muscle

A

Proteolysis to from AA from protein

Ketogenesis to form ketone bodies from FA

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12
Q

Which pathways used during Fed/fasting/starving state in heart

A

B-oxidation of fatty acids during fed/fasting

Ketone bodies used in TCA cycle during starvation

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13
Q

Which pathways used during fed/fasting/starving state in brain

A

Glucose used in glycolysis/TCA cycle during fed/fasting

Ketone bodies used in TCA cycle during starvation

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14
Q

Which pathways used during fed/fasting/starving state in adipose tissue

A

Fed- Fatty acids–>TAGs

Fasting/Starving- TAGs–> fatty acids/glycerol (lipolysis)

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15
Q

AMPK during fed state is active/inactive

A

Inactive

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16
Q

What are activators/inhibitors of AMPK

A

AMP activates

ATP inhibits

17
Q

AMPK activates enzymes in what pathways and deactivates enzymes in what other pathways

A

Activates enzymes in energy producing (catabolic) pathways

Deactivates enzymes in energy requiring (anabolic) pathways

18
Q

mTOR activation state when fed

A

Activated in fed state

19
Q

mTOR activators/inhibitors

A

Activated by insulin

Inhibited by AMPK

20
Q

mTOR activates/deactivates enzymes in which pathways

A

Activates in energy requiring (anabolic) pathways

Deactivates in energy producing (catabolic) pathways

21
Q

AMPK can bind how many ATPs

22
Q

Origin/destination/role of chylomicrons

A

O- Intestine
D- Adipocytes
Role- TAG transport

23
Q

Origin/destination/role of VLDL

A

O- Liver
D- Adipocytes
Role- TAG transport

24
Q

Origin/destination/role of IDL

A

O- VLDL
D- Liver, adipocytes
Role- Intermediate molecule

25
Origin/destination/role of LDL
O- VLDL D- All cells Role- Cholesterol distribution
26
Origin/destination/role of HDL
O- Liver (empty) D- Liver (full) Role- Cholesterol collection
27
What do sirtuins do and when are they activated
Deacetylate Lysine using NAD+ | Activated when NAD is high and NADH is low
28
Role of leptin
Released from adipocytes to signal the brain that you are full. Senses storage of TAGs
29
What hormones are similar to leptin but only act briefly
CCK | GLP1
30
Leptin/Insulin effect on mTOR and AMPK
Leptin/insulin both activate mTOR | Leptin inhibits AMPK
31
Ghrelin/adiponectin effect on AMPK
Both activate AMPK
32
Orexigenic neurons disseminate hungry signals from
Ghrelin Adiponectin PYY3-36
33
Anorexigenic neurons disseminate fed/full signals from
Leptin/insulin
34
Cortisol effects on adipocytes/skeletal muscle/liver
Adipocytes- Release FA Skeletal muscle- Protein degradation, export AAs Liver- increased pyruvate carboxylase and gluconeogenesis action