16 Flashcards

1
Q

whats long term energy storage source

A

lipids

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2
Q

how does fat get converted to energy

A
  1. TAG goes into diaglycerol via ATGL then to FA and glycerol via hormone sensitive lipase triggered by glucagon and adrenaline increase.

breakdown using lipolysis where FA can be oxidised for energy in oxidisive tissues or converted to ketone bodies in non oxidative tissue

glycerol can be used for glucose synthesis

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3
Q

what triggers hormone sensitive lipase

A

adrenaline

glucagon

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4
Q

would you still get glycerol and FA if you knock out DAG

A

yes but less so

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5
Q

how do FA get oxidised

A
  1. FA gets acitvated by acetylcoA to fatty acylcoA
  2. fatty acylcoA goes inside mitochondria via CPT 1 and CPT 2
  3. beta oxidation to go from fatty acylcoA to acetyl coA and NAD for electron transport chain
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6
Q

how doe acetyl coA activate FA

A

by attaching coa

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7
Q

how does fattyacyl coa get to mitochondria

A

via carnitine shuttle

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8
Q

where does beta oxidation are place

A

mitochondria

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9
Q

what enzymes does beta oxidation of fatty acids (acetylCoa)

A

acetylcoA dehydrogrenases

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10
Q

where does beta oxidation not happen

A

brain and rbc

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11
Q

b oxidation removes how many carbons at a time

A

2

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12
Q

what controls catabolism of FA

A

the point of control is tranport to mitochondria. CPT inhibited by malonylcoA

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13
Q

whats the level. of CPT1 during starvation

A

high

bc activated by glucagon

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14
Q

can fats be used for gluconeogeneiss

A

no but you can use product of beta oxidation which is acetylcoA

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15
Q

ok so how does the body actually make fat

A

in cytoplasm by adding two carbon units.
in time sof plenty, you have glucose goes to pyruvate… you have a lot of citrate so you can take citrate to cytoplasm where its broken down to acetylcoA
enzyme acetylcoA carboxylase takes you from acCoA to Mal Coa which is then used to add 2 carbon units onto growing FA chains. losing Co2 in the process.

so two stgaes
one is formation of malonylcoa
formation of fatty acid chain

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16
Q

at what stage is fatty acid synthesis controlled

A

when acetylcoacarboxylase turns acccoa to malonyl

17
Q

how is acetylcarboxylase controlled

A

polymerization turns on
phosphorylation (turn off)
long term genetic control

18
Q

brain doesn’t do beta ox. brain cant use fat. so what happens when there’s no glucose

A

ketone bodies.

19
Q

ketone body ancestor

A

acetylcoa made by beta ox in liver

20
Q

how are ketone bodies produced

A

you join acetylcoA and
acetoacetate which makes HMG CoA synthase.

that goes into b hydroxytbu dhkhdjks are then taken to the bood
if well fed. you wont have much HMG CoAsynthesase

21
Q

how is ketone body production controlled

A

postranslational modification: acetylation

transcriptionally. FOXA2 and PPARalpha

22
Q

whats the main regulatory step in ketone body production

A

making HMG CoA synthase

23
Q

how are ketone bodies used

A

converted back to acetylcoa and used for TCA cycle

24
Q

can liver oxidise so use ketone bodies

A

no

25
Q

whats the effect of insulin on ketone bodies

A

insulin inhibits production of ketone bodies.

26
Q

whats the relationship entre diabetes and ketone

A

diabetes have too little insulin so too much ketone so diabetic ketoacidosis ensues.

27
Q

what kind of modification regulates the conversion of pyruvate to acetyl coa at the end of glycolysis

A

covalent through phosphorylation by both PDH kinase and a protein kinase A

28
Q

what inhibits fat oxidation when theres a lot of glucose

A

malonyl coa

29
Q

whats metabolic flexibility

A

ability to switch from glucose to lipid metabolism

higher ability in fit people