Integration of Metabolism Flashcards

1
Q

what are the 3 main decisions in the reductionist approach ?

A

what to do with the following:

  1. G6P
  2. pyruvate
  3. acetyl coa
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2
Q

G6P uses

A

convert to:

  1. G1P to create glycogen
  2. thru PPP to create R5P
  3. F6P to create pyruvate
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3
Q

what can pyruvate be converted into?

A

acetyl coa
alanine
lactate
OAA

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4
Q

fates of acetyl CoA

A
  1. enter ketone body synthesis
  2. FA synthesis
  3. TCA or OxPhos cycle
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5
Q

brain

A

no fuel reserve

wants glucose
—use ketones in starvation

does not export fuel

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6
Q

skeletal muscle during rest

A

glycogen, protein reserves

wants fatty acids

does not export fuel

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7
Q

skeletal muscle during activity

A

no reserves

uses glucose

exports lactate

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8
Q

heart muscle

A

no reserves

wants fatty acids

does not export

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9
Q

adipose tissue

A

TAG reserves

wants to use fatty acids

exports fatty acids and glycerol

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10
Q

liver

A

reserves = glycogen, TAGs

uses glucose, FAs, AAs

exports: FAs, glucose, ketone bodies

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11
Q

what are the main fuel producers of the body

A

liver - glucose
adipose - FAs
kidneys - glucose during starvation only

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12
Q

what are the main fuel consumers of the body

A

skeletal muscle
glycogen —> creatine Pi —> lactate

brain
glucose —> ketones

heart
FAs —> lactate/ketones

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13
Q

significance of liver lacking CoA transferase

A

it can produce but not use ketone bodies

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14
Q

organs containing the urea cycle

A

liver

kidneys

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15
Q

LDL

A

origin - vldl

destination - all cells

role – cholesterol distribution

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16
Q

HDL

A

origin - empty liver
destination - full liver

role - cholesterol collection

17
Q

VLDL

A

origin - liver
destination - adipose

role - TAG transport

18
Q

chylomicron

A

origin - intestine
destination - adipose

role - TAG transport

19
Q

diabetes mimics _____ conditions

A

starvation conditions

the insulin deficiency blocks entry of glucose into muscle and adipose cells

problems w/ the insulin receptor - its never put out on memb of cells
or
insulin is never produced

20
Q

enzyme regulators of metabolism

A

AMPK and mTOR
serine/threonine kinases w/ opposite functions

mTOR increases synthesis pathways - on in fed state
AMPK inhibits it

21
Q

enzyme metabolism regulators - sirtuins

A

deacetylate lysine

use NAD+
redox rxn
activated when [NAD+] is high

22
Q

metabolism regulators - hormones

A
insulin
glucagon
epinephrine
leptin
ghrelin
PYY3-36
adiponectin
23
Q

insulin

A

released from pancreas

acts in fed state
tells cells to uptake glucose

24
Q

leptin

A

released from adipose

acts in full state
meant to tell you you’re full

25
Q

CCK and GLP1 plus leptin

A

all act in full state to tell you to stop eating

but leptin in long lasting
others are short

26
Q

hungry signals

A

ghrelin
adiponectin
PYY3-36

27
Q

cortisol

A
slow acting
periods of chronic stress
a cholesterol derivative
tissue specific actions:
adipose --- release FAs
skeletal --- protein catabolism
liver --- increase gluconeogenesis