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
CCK and GLP1 plus leptin
all act in full state to tell you to stop eating but leptin in long lasting others are short
26
hungry signals
ghrelin adiponectin PYY3-36
27
cortisol
``` slow acting periods of chronic stress a cholesterol derivative tissue specific actions: adipose --- release FAs skeletal --- protein catabolism liver --- increase gluconeogenesis ```