glucokinase, PFK1, and pyruvate kinase
enzymes found in glycolysis but not gluconeogenesis
-Lactate (pyruvate) - Cori cycle
-Gluconeogenic amino acids (all, except leucine and lysine)
-Glycerol (from the breakdown of triglycerides)
-All TCA intermediates (not acetyl-CoA)
major gluconeogenic organ
location of gluconeogenesis
primarily in the cytosol, but some precursors are made in the mitochondria (place)
gluconeogenesis does not occur in
muscle cells because they lack glucose 6-phosphatase or glucagon receptors
gluconeogenesis is stimulated by
falling levels of glucose, increased glucagon levels, decreased insulin levels
glycolysis and gluconeogenesis is regulated by
electron shuttle that turns lactate into pyruvate
used in decarboxylation reactions
used in carboxylation reactions
electron shuttle required for gluconeogenesis
makes NADH if lactate is the carbon source
Where does gluconeogenesis get NADH if alanine is the carbon source?
ethanol effect on gluconeogenesis
It increases NADH levels, which inhibits the conversion of lactate to pyruvate, thus inhibiting gluconeogenesis
major regulator of gluconeogenesis
conversion of fructose 1,6-phosphate to fructose 6-bisphosphate
How is the PFK-1 reaction bypassed?
in a simple hydrolytic reaction catalyzed by fructose 1,6-bisphosphatase
How is the glucokinase reaction bypassed?
in a simple hydrolysis reaction catalyzed by glucose 6-phosphatase
Where is glucose 6-phosphatase located?
On the ER and found only in the liver
Where do the carbon atoms for gluconeogenesis come from?
lactate or amino acids
fatty acid oxidation
What provides the necessary energy for gluconeogenesis?
major allosteric modulator of PFK-1 and fructose 1,6-bisphosphatase?
Regulates fructose 2,6-bisphosphate production; not active when phosphorylated
What happens when PFK-2 is inhibited?
-leads to low levels of fructose 2,6-bisphosphate, which inactivates PFK-1 and activates fructose 1,6-bisphosphatase
cofactor for carboxylation enzymes
What are the metabolic consequences of biotin deficiency?
accumulation of lactate, acetyl CoA, and ketones (diabetic ketoacidosis); failure in fatty acid synthesis, developmental retardation, lethargy, hallucinations, rash