Nutritional status-Metabolic Pathways Flashcards
Allosteric Effectors
-Acetyl-CoA, AMP, Citrate, Fructose 2,6 BP, Fructose 1,6 BP, Glucose, Malonyl-CoA
Acetyl CoA
- signals–>availability of CoA
- affects
- ->activates pyruvate carboxylase (gluconeogenesis),
- ->inhibits pyruvate dehydrogenase
AMP
- signals–>low energy charge
- affects–>activates glycogen phosphorylase (glycogen degradation) and PFK1
Citrate
- signals–>availability of acetyl-CoA
- affects–>activates acetyl-CoA carboxylase (FA synthesis)
- ->inhibits PFK1 and PFK2 (glycolysis)
Frustose 2,6 BP
- signals–>availability of glucose
- affects–>activates PFK1 and inhibits F 1,6 BPase
Fructose 1, 6 BP
- signals–>availablity of glucose
- affects–>activates pyruvate kinase
Glucose
- signals–>availability of glucose
- affects–>activates glucokinase (indirectly, translocation from nucleus into cytoplasm)
Malonyl-CoA
- signals–>FA synthesis
- affects–>inhibits CPT 1 (FA degradation)
Protein Phosphorylation
-AMP & cAMP
AMP
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
cAMP
- signals–>starvation-low glucose
- affects–>Activates protein kinase A, leads to phosphory-lation of key enzymes
- Increases glycogenolysis
- Increases gluconeogenesis
- Inhibits glycolysis
- Inhibits lipogenesis
Protein expression stimulus
-fatty acids, glucagon, insulin
Fatty acids
- signals–>starvation (lipolysis)
- affects–>Induce genes for fatty acid oxidation and ketone synthesis via peroxisome proliferation response element (PPRE)
Glucagon
-signals–>starvation
-affects–>Induces genes for gluconeogenesis via CREB-binding element (CRE)
Represses genes for lipid synthesis via CRE
Insulin
-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)