Regulators/Regulatory Mechanisms Flashcards
Acetyl-CoA Carboxylase (ACC)
biotin requiring enzyme
allosteric activator = citrate
allosteric inhibitor = long chain fatty acyl-CoA
DePhosphorylation = high I/G = Active
Phosphorylation by AMP-Kinase (AMPK) = inactive
Sterol-dependent regulation via SRE and SREBP
-Insulin signal leads to the proteolytic cleavge of SREBP from ER (release of SREBP) resulting in the ACC gene expression and lipogenesis
Glucagon and dietary PUFAs prevent release of SREBP resulting in decrease in ACC and lipogen
citrate
+ ACC (polymerization)
+ ATP-Citrate Lyase (feed forward)
- PFK-1
- citrate snythase
Fructose-2,6-bisPhosphate and AMP
+ PFK1
- FBPase1
Calcium
+ PDH Phosphatase (which activates PDHC via dephosphorylation)
+ Isocitrate dehydrogenase
+ KGDHC
+ glycogenolysis
Acetyl-CoA
+ pyruvate carboxylase (TCA Priming/ gluconeogenesis)
+ PDH Kinase (which inhibits PDHC via phosphorylation)
+ mitochondrial HMG-CoA synthase (ketogenesis)
F-1,6-BP
+ pyruvate kinase (feed forward)
Malonyl CoA
- CPT-1 (fatty acid oxidation
cholic acid
- cholesterol 7-a-hydroxylase
NADH
- Isocitrate Dehydrogenase
- KGDHC
- PDHC
+ PDH Kinase (Which phosphorylates PDHC and inactivates PDHC)
AMPK
phosphorylates ACC (inhibits lipogenesis) AMPK will elevate F-2,6-BP production during circulatory system collapse
ATP
+ PDH Kinase (which phosphorylates and inactivates PDHC)
- Isocitrate dehydrogenase
+ FBPase1
PUFAs
decrease release of SREBP
decrease gene expression of ACC and HMG-CoA reductase
High I/G/Fed, & what is the covalent modification status
DEPHOSPHORYLATION
+ Pyruvate Kinase (glycolysis)
+ Acetyl-CoA carboxylase (de nova FA snyth)
+ HMG-CoA Reductase (de novo cholesterol snth)
+ Glycogen Synthase A (glycogenesis)
+ PDHC
+ PFK-2 (making more F-2,6-BP which activates PFK1) (Glycolysis)
Fast (Low I/G / high epinephrine)
Phosphorylation
+hormone-sensitive lipase
+glycogen phosphorylase a (glycogenolysis)
+ FBP-2 (which decreases F-2,6-BP, which would otherwise allosterically activate PFK1)
Oversupply of cholesterol
- Synthesis of LDL receptors
- HMG-Coa reductase (ie synthesis cholesterol) (regulation via SREBP)
+ ACAT (which takes cholesterol and makes cholesterol esters for storage
+ cholesterol 7a-hydroxylase