Biochemistry

Front 1

krebs cycle is controlled early on, at which components?

Back 1

isocitrate dehydrogenase (ICDH) and alpha-ketoglutarate dehydrogenase (KGDH/OGDH)

Front 2

what is a dehydrogenase?

Back 2

A dehydrogenase is an enzyme that oxidizes a substrate by transferring one or more protons and a pair of electrons to an acceptor, usually NAD/NADP or a flavin coenzyme such as FAD

Front 3

what stimulates isocitrate dehydrogenase (ICDH) and alphaketoglutarate dehydrogenase (KGDH/OGDH)?

Back 3

a rise in calcium concentration (such as is found during exercise)

Front 4

true or false: exercise can stimulate the krebs cycle?

Back 4

true. increasing calcium concentration (muscle contraction) stimulates ICDH and OGDH

Front 5

what are ICDH and OGDH sensitive to?

Back 5

calcium levels, NAD levels (can't work unless NAD is available), ATP levels

Front 6

providing more enzymes (ICDH and OGDH) only works to make the krebs cycle faster if. . .

Back 6

more carrier (oxaloacete) is provided. ie need more oxaloacetate during exercise

Front 7

what is an anaplerotic reaction?

Back 7

Anaplerotic reactions are those that form intermediates of the citric acid cycle which can be used to 'top up' the whole cycle

Front 8

can muscle make extra oxaloacetate?

Back 8

yes, in muscle pyruvate carboxylase supplies extra oxaloacetate from pyruvate (anapleurotic reaction) so not only the liver has pyruvate carboxylase

Front 9

does only the liver have pyruvate carboxylase?

Back 9

no, muscle has it too

Front 10

in the krebs cycle, when do you get a release of CoA?

Back 10

when acetyl CoA comes into the krebs cycle and is converted into citrate CoA is released

Front 11

what does fatty acid oxidation require a source of?

Back 11

CoA

Front 12

what is another name for fatty oxidation?

Back 12

beta-oxidation (because the action occurs on the beta-carbon)

Front 13

what are the three steps, from succinate to oxaloacetate that are the same in fatty acid oxidation?

Back 13

(CH2 going to C=O)
-oxidation with FAD
-hydration
-oxidation with NAD

Front 14

where does fatty acid oxidation occur?

Back 14

mitochondria

Front 15

what's the relationship between the rate of fatty acid oxidation and glucose oxidation?

Back 15

reciprocal - opposite to each other (fatty acid oxidation inhibits glucose oxidation, insulin inhibits fatty acid oxidation)

Front 16

what does fatty acid oxidation inhibit?

Back 16

glucose oxidation

Front 17

what does hormone insulin (glucose oxidation favoured) inhibit?

Back 17

fatty acid oxidation

Front 18

what does fatty acid oxidation consume?

Back 18

a lot of FAD, NAD, CoA therefore these cofactors have to be available. if any of them are lacking, the rate of fatty acid oxidation will be compromised

Front 19

fatty acids don't tend to exist 'naked'. in the bloodstream what are fatty acids complexed with?

Back 19

albumin

Front 20

how do you 'trap' fatty acids in a cell?

Back 20

attach CoA to them

Front 21

how do fatty acids get transported from the blood into the cytoplasm?

Back 21

bind to albumin to cross into cytoplasm through a transporter (which facilitates diffusion). FA bind to FAprotein (soaks up FA) then attached to CoA (to trap FA inside cell)

Front 22

what are fatty acids bound to in cytoplasm?

Back 22

fatty acid binding protein

Front 23

what are fatty acids bound to in blood?

Back 23

albumin

Front 24

how does albumin bind to fatty acids?

Back 24

albumin has several fatty acid binding sites

Front 25

what's an example of a specific fatty acid transporter and what does it do?

Back 25

CD36 (FATP). it moves to the cell surface whenever there is a need to take up FA at a rapid rate.

Front 26

how do you 'trap' fatty acid with CoA and what does it do?

Back 26

have to invest energy (ATP to AMP and 2Pi). CoA is big and charged, can't get across membranes, it traps FA inside cytoplasm and activates (primes) FA

Front 27

what is the functional part of CoA?

Back 27

the HS group which forms thioesters with fatty acids

Front 28

how do you get fatty acids out of the cytoplasm and into the mitochondria?

Back 28

'piggy backs' FA on carnitine, ferries FA-carnitine across membrane

Front 29

what is the enzyme that catalyses FA binding to carnitine?

Back 29

carnitine acyl transpirase (CAT-1)

Front 30

are the CoA from the cytoplasm the same as the CoA from the mitochondrial matrix?

Back 30

no, CoA made in both cytoplasm and matrix, the 2 CoAs never meet (can't cross membrane)

Front 31

what happens to FA-carnitine made in the cytoplasm?

Back 31

the whold complex passes into the matrix (with help of carrier) then CoA (mitochondrial) binds to FA catalysed by CAT-2 and free carnitine passes back into the cytoplasm

Front 32

what can inhibit the enzyme CAT-1 and what is the effect?

Back 32

malonyl CoA. stops fatty acids from getting into mitochondrial matrix - inhibition of fat oxidation

Front 33

what is the only fate for fatty acids once they get into the mitochondria?

Back 33

fatty acid oxidation

Front 34

what can happen to FA-CoA in the cytoplasm?

Back 34

made into fat/lipid through esterification with glycerol-3-phosphate

Front 35

what does insulin inhibit?

Back 35

FA-CoA becoming FA-carnitine

Front 36

what do you NEED for fatty acid oxidation?

Back 36

CoA, FAD, NAD

Front 37

what does fatty acid oxidation make?

Back 37

acetyl-CoA, NADH, FADH2
and an oxidised fatty acid less 2 carbons than starting product