Integrating Carbs/lipids

Front 1

3 important molecules that are crossroads in lipid/carb metabolism:

Back 1

-Glucose 6 phosphate
-AcCoA
-Pyruvate

Front 2

5 main enzymes under allosteric control:

Back 2

Glycolysis: PFK1, FBPase
FA Biosnth: AcCoA Carboxylase
Pyruvate: PDH
Pyruvate: Pyruvate Carboxylase

Front 3

Allosteric effectors of PFK1:

Back 3

Negative: Citrate (sends G6P to gluconeogenesis instead)
Negative: ATP

Positive: F26BP

Front 4

Allosteric effectors of FBPase1:

Back 4

Negative: F26BP

Positive: ATP

Front 5

Result of active PFK1:

Back 5

Glycolysis

Front 6

Result of active FBPase1:

Back 6

Gluconeogenesis

Front 7

Allosteric effectors of AcCoA Carboxylase:

Back 7

Positive: Citrate

Front 8

Allosteric effector PRODUCED BY AcCoA Carboxylase:

Back 8

Malonyl CoA

Front 9

Effect of Malonyl CoA

Back 9

Inhibits CPT1 - turns off FA b-oxidation

Front 10

Allosteric effectors of PDH:

Back 10

-Neg Feedback of NADH, AcCoA

Front 11

NADH inhibits:

Back 11

-PDH
-TCA Isocitrate dehydrogenase
-TCA Aketoglutarate dehydrogense

Front 12

Allosteric effectors of Pyruvate Carboxylase

Back 12

AcCoA Activates it
(as PDH is turned off AcCoA shuttles into gluconeogenesis)

Front 13

What allows Covalent regulation?

Back 13

Glucagon:insulin ratio

Front 14

Glucagon phosphorylation will ACTIVATE 3 things:

Back 14

-Glycogen phosphorylase (use glycogen stores)
-FBPase2 (turn off glycolysis)
-Hormone sensitive Lipase (HSL)
(turn on

Front 15

Glucagon phosphorylation will INACTIVATE 3 things:

Back 15

-Glycogen synthase
-PFK2
-Pyruvate kinase

Front 16

AMPK

Back 16

special phosphorylator for AcCoA Carboxylase

Front 17

What activates AMPK

Back 17

AMP

Front 18

What is the effect of AMPK:

Back 18

Phosphorylation = inactive AcCoA Carboxylase -> no FA biosynth

Front 19

Molecule that counteracts the effect of AMPK to some degree:

Back 19

Citrate - if it's building up from TCA, will shuttle to cytosol and allow FA biosynth in spite of high AMP levels.

Front 20

Covalent regulation of PDH

Back 20

-Personal phosphorylator
-Inactivates E1

Front 21

What activates the phosphorylator of PDH?

Back 21

-AcCoA
-NADH
-ATP

Front 22

So the effect of High energy on Pyruvate pools:

Back 22

1. Kinase phosphorylates PDH (-)
2. Pyruvate not used by TCA
3. Shuttle to gluconeogenesis

Front 23

Effect of LOW energy on pyruvate pools:

Back 23

1. Kinase inactive; PDH +
2. TCA works

Front 24

Long term Regulation of gluconeogenesis:

Back 24

PEPCK gene

Front 25

How is PEPCK gene regulated?

Back 25

-Responds to binding elements (Ins/Cort/Epi/cAMP)
-Changes concentration of enzyme

Front 26

What allows for coordinated regulation of many pathway enzymes at once?

Back 26

SRE - serum response element

Front 27

4 enzymes controlled by SRE for FA biosynthesis:

Back 27

1. ATP-Citrate Lyase
2. Malic enzyme
3. AcCoA Carboxylase
4. FAS (FA Synthase)

Front 28

2 reactions of TCA shut off by NADH:
(what else turns them off?)

Back 28

1. Isocitrate Dehydrog
2. a-Ketoglutarate Dehydrog

(Incr ATP/ADP turns off too)

Front 29

3 Pathways in Cytosol:

Back 29

1. Glycolysis
2. FA Biosynth
3. PPP

Front 30

4 Pathways in Mitochondria

Back 30

1. FA oxidation
2. TCA
3. Oxidative phosphorylation
4. Ketone formation

Front 31

2 Pathways that interplay between mito and cyto:

Back 31

1. Gluconeogenesis
2. Urea synthesis

Front 32

How AcCoA pool converts from TCA to gluconeogenesis:

Back 32

AcCoA activates Pyruvate Carboxylase

Front 33

What does Pyruvate Carboxylase do?

Back 33

AcCoA -> Oxaloacetate that gets sent to cytosol for gluconeogenesis or ketogenesis.

Front 34

What molecule is specific for adipocytes and involved in Fat mobilization?

Back 34

HSL - hormone sensitive lipase

Front 35

What activates HSL?

Back 35

Glucagon/cAMP/PKA phosphorylation

Front 36

What is the effect of insulin on HSL?

Back 36

Inactive - if you're fed you don't need to be using your fat stores.