Nutritional status-Metabolic Pathways Flashcards

1
Q

Allosteric Effectors

A

-Acetyl-CoA, AMP, Citrate, Fructose 2,6 BP, Fructose 1,6 BP, Glucose, Malonyl-CoA

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2
Q

Acetyl CoA

A
  • signals–>availability of CoA
  • affects
  • ->activates pyruvate carboxylase (gluconeogenesis),
  • ->inhibits pyruvate dehydrogenase
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3
Q

AMP

A
  • signals–>low energy charge

- affects–>activates glycogen phosphorylase (glycogen degradation) and PFK1

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4
Q

Citrate

A
  • signals–>availability of acetyl-CoA
  • affects–>activates acetyl-CoA carboxylase (FA synthesis)
  • ->inhibits PFK1 and PFK2 (glycolysis)
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5
Q

Frustose 2,6 BP

A
  • signals–>availability of glucose

- affects–>activates PFK1 and inhibits F 1,6 BPase

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6
Q

Fructose 1, 6 BP

A
  • signals–>availablity of glucose

- affects–>activates pyruvate kinase

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7
Q

Glucose

A
  • signals–>availability of glucose

- affects–>activates glucokinase (indirectly, translocation from nucleus into cytoplasm)

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8
Q

Malonyl-CoA

A
  • signals–>FA synthesis

- affects–>inhibits CPT 1 (FA degradation)

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9
Q

Protein Phosphorylation

A

-AMP & cAMP

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10
Q

AMP

A

signals–>low energy charge

  • affects–>Activates AMP dependent kinase AMPK, leads to phosphorylation of key enzymes
  • Inhibits gluconeogenesis
  • Inhibits protein synthesis
  • Inhibits lipogenesis
  • Inhibits cholesterol synthesis
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11
Q

cAMP

A
  • signals–>starvation-low glucose
  • affects–>Activates protein kinase A, leads to phosphory-lation of key enzymes
  • Increases glycogenolysis
  • Increases gluconeogenesis
  • Inhibits glycolysis
  • Inhibits lipogenesis
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12
Q

Protein expression stimulus

A

-fatty acids, glucagon, insulin

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13
Q

Fatty acids

A
  • signals–>starvation (lipolysis)
  • affects–>Induce genes for fatty acid oxidation and ketone synthesis via peroxisome proliferation response element (PPRE)
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14
Q

Glucagon

A

-signals–>starvation
-affects–>Induces genes for gluconeogenesis via CREB-binding element (CRE)
Represses genes for lipid synthesis via CRE

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15
Q

Insulin

A

-signals–>well-fed state
-affects–>Induces genes for lipid synthesis via SREBP-1c responsive element (SRE)
Represses genes for gluconeogenesis and FA oxidation via insulin response element (IRE)

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