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Biochem Block 2 > GNG > Flashcards

GNG Flashcards

1
Q

Gluconeogenesis

A
  • GNG
  • Metabolic pathway that results in the generation of glucose from non-carbohydrate precursors
  • Anabolic
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2
Q

GNG purpose

A

-to maintain blood glucose levels and avoid hypoglycemia under conditions of fasting(more than 10-18 hours)

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3
Q

What organs is GNG?

A
  • Liver:predominantly

- Kidney cortex: at lesser extent, only during prolonges fasting contribute up to 40% of total glucose production

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4
Q

Where in cell is GNG?

A

Step 1: mitochondrial matrix
Middle steps: all reversible steps of glycolysis
Last Step: ER

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5
Q

Substrates for GNG

A

glycerol

  • AA
  • lactate
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6
Q

Glycerol

A
  • release during hydrolysis of TAGs in adipocytes and is delivered by the blood to liver
  • adipocytes lack glycerol kinase
  • only in the liver: glycerol—>glycerol P—>DHAP
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7
Q

Amino Acids

A
  • major source are AA derived from tissue protein hydrolysis(use muscle mass in times of starvation)
  • Alanine is major AA used, but most can be
  • Most AA are converted in the TCA to intermediates that can yield OAA at some point
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8
Q

Lactate

A

-can be converted back into pyruvate in the liver by lactate dehydrogenase(enzyme is only in the liver. lactate from RBC to liver to be converted and avoid build up)

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9
Q

Cori Cycle

A
  • -glucose converted into lactate under anaerobic glycolysis
  • excreted to plasma
  • sent to liver to be converted back to glucose
  • released back into circulation
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10
Q

Acetly CoA

A
  • CANNOT BE CONVERTED TO PYRUVATE IN HUMANS

- PDH is irreversible

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11
Q

Fatty Acids

A
  • FA cannot be used as substrate for GNG

- FA oxidation provides the liver with the energy required to perform GNG

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12
Q

reversible steps of GNG

A
  • 7 reversible steps from glycolysis

- highly dependent on concentration of substrates and products

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13
Q

Carboxylation of pyruvate to OAA(part 1)

A
  • in mitochondrial matrix
  • provide OAA for GNG and TCA replinishment
  • pyruvate can’t go into mitochondria
  • requires Biotin as coenzyme
  • allosterically activated by acetyl CoA
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14
Q

Biotin/Bicarbonate

A
  • biocarbonate ion is not free floating, attached to CO2

- biotin is bound to pyruvate carboxylase so biocarbonate ion can attach and release C for pyruvate

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15
Q

Carboxylation of pyruvate to OAA(part 2)

A
  • OAA cant be exported so, converted to malate
  • malate goes through to cytosol and is oxidatively decarboxylated back to OAA
  • malate dehydrogenase and PEP carboxykinase
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16
Q

Decarboxylation of cytosolic OAA

A
  • irreversible
  • driven by GTP hydrolysis
  • pairing carboxylation with decarboxylation makes GNG energetically possible
  • PEPCK
  • remove one C from OAA and add P
17
Q

Dephosphorylation of fructose 1,6-bisphosphate

A

-hydrolysis reaction
-bypass the irreversible PFK-1 reaction
-important site for regulation
fructose 1,6-bisphosphatase

18
Q

Regulation of Fructose 1,6-bisphosphatase

A
  • high AMP levels inhibit
  • allosterically inhibited by fructose 2,6-bisphosphate
    • activator of PFK-1, made by PFK-2
    • common regulator shows glycolysis and GNG are mutually exclusive
  • Activated by high ATP
19
Q

Dephosphorylation of glucose 6-P

A
  • removal of P to free glucose and let it exit
  • hydrolysis reaction
  • bypass hexokinase irreversible reaction
  • provides energetically favorable step to produce glucose
  • GLUCOSE 6-PHOSPHATASE
  • enzyme faces lumen so it can cleave glucose before it leaves
20
Q

Von Gierke disease

A

-glucose 6-phosphatase deficiency

21
Q

Energy summary of GNG

A
  • endergonic pathway
  • anabolic pathway
  • for 1 glucose,
  • 4 ATP and 2 GTP used
  • 2 NADH are used
22
Q

Regulation by glucagon

A
  • inhibits PFK-2, lowers fructose 2,6-bisposphate
  • inhibits pyruvate kinase so PEP is used for GNG and not glycolysis
  • stimulates transcription of PEPCK to activate it
  • inhibits glycolysis, activates GNG
23
Q

Regulation by substrate availability

A
  • protein breakdown in other tissues and AA release yields gluconeogenic precursors in the liver
  • stimulates GNG
  • ATP and NADH are provided by the oxidation of fatty acids in liver
24
Q

Allosteric activation by acetyl CoA

A
  • build up of acetyl CoA signials diversion of OAA for GNG
  • activates pyruvate carboxylase
  • inhibits PDH so pyruvate goes to GNG and not TCA
25
Q

Allosteric inhibition by AMP

A
  • fructose 1,6-bisphosphatase is inhibited by high AMP
  • PFK-1 activated by High AMP
  • assures two pathways are mutually exclussive

Biochem Block 2 (11 decks)

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