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Flashcards in BC 30 Deck (11)
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1
Q

Metabolic Priorities for Liver in Fasting State (5-24)

A
  1. FA Oxication (TCA and ETC) for hepatocytes own energy needs

Service Acts
1)Ketogenesis-utilize surplus acetyl coA to generate ketone bodies for export

2) Glycogenolysis (BG homeostasis)
3) gluconeogenesis, utilize C skeletons from amino acids

2
Q

Protein sparing compounds and associated state

A

Fed state: dietary carbs

Short fast: Liver glycogen

Long fast: Ketone bodies

3
Q

What three glycolysis reactions are irreversible and must be circumvented

A

Pyruvate Kinase,
PFK 1
Glucokinase

4
Q

liver vs Renal Gluconeogenesis for bodies needs

A

Short term fasting

  • liver 90%
  • kidney 10%

long term fasting

  • liver 50%
  • kidney 50%
5
Q

gluconeogenesis steps

A

Pyruvate –>OAA by Pyruvate Carboxylase

Shuttle out of Mito
OAA–>Malate by NADH
-exits Mitochondrial membrane
Malate–>OAA by NAD+

OAA–>phosphoenol pyruvate (PEP Carboxykinase)
-several more reversible reactions to F16BP

F16BP–> F6P by FBPase1

  • RATE LIMITING
  • how do FBPase1 and FBPase relate?
  • F6P to G6P reversible reaction

G6P–>Free Glucose by Glucose 6 Phosphatase
-ONLY IN LIVER and kidney cortex

6
Q

Cori Cycle

A

cyclic catabolism of glucose/lactate in RBC and Muscle and gluconeogenesis in liver

-significance: shift in metabolic burden of breakdown from those tissues to the liver

Gluconeogenesis will also only run if sufficient ATP and Precursors are present (glycogenic AA or lactate)

  • lactate from RBC and exercise
  • –both in anaerobic conditions
7
Q

Step One Gluconeogenesis

A

Pyruvate –> OAA by pyruvate carboxylase

Puts a CO2 on pyruvate to make OAA. Same reaction used for the TCA priming

  • Allosterically regulated by mitochondrial AcCOA
  • -Increased AcCoA activates PC (inh PDHC)
  • -AcCoA increased in fasting due to FA ox

ATP consumption-activation and transfer of CO2 by biotin coenzyme during caboxylation of pyruvate.
-all carboxylases require biotin coenzyme, provides the binding of CO2

8
Q

OAA shuttle out side IMM

A

OAA unable to cross IMM
reduced to Malate by NADH

malate passes through

oxidized to OAA by NAD+

9
Q

Step 2 Gluconeogenesis

A

OAA–>PPPy by PEP Carboxykinase (HYDROLIZE GTP)
-carboxylates and phosphorylates OAA

-more reversible reactions to F16BP

10
Q

Step 3 Gluconeogenesis

A

F16BP–>F6P by Fructose Bisphosphatase
-RATE LIMITING STEP

can be allosterically regulated: FBPase inhibited by AMP and F26BP (allosteric activator of PFK1)

Hormonally regulated

  • F26BP levels regulated by IG ratio via combo enzyme PFK2/FBP2
  • increased IG increase cAMP increase PKA and phosphorylates PFK2 inactivating it. FBP2 active decreasing F26BP increasing gluconeogenesis
  • reciprocal hormone regulation F26BP increased by PFK2
11
Q

Step 4 Gluconeogenesis

A

G6P enzyme shared with glycogenolysis

  • ONLY IN LIVER
  • G6P–>free glucose (dephosphorylation)

freed to blood