Metabolism V Flashcards
How to ATP synthase inhibitors poison the ETC?
Directly inhibit mitochondrial ATPsynthase causing an increased proton gradient. ATP cant be produced because electron transport stops alltogether (p.102)
Name one ATP synthase inhibitor.
Oligomycin (p.102)
How to ATP uncoupling agents poison the ETC?
Increase the permeability of the membrane causing a decreased proton gradient and increased oxygen consumption. ATP synthesis stops but electron transport continues and heat is produced (p.102)
Give three examples of an ETC uncoupling agent.
2,4-DNP, aspirin (fevers often accompany asprin overdose), thermogenin in brown fat (p.102)
Name the four irreversible enzymes in gluconeogenesis.
Pyruvate carboxylase, PEP carboxykinase, Fructose 1,6-bisphosphatase, Glucose-6-phosphatase (p.102)
What reaction is catalyzed by pyruvate carboxylase and where does the reaction occur?
Pyruvate –> oxaloacetate. Reaction occurs in the mitochondria (p.102)
What reaction is catalyzed by PEP carboxykinase and where does the reaction occur?
Oxaloacetate –> Phosphoenolpyruvate. Reaction occurs in the cytosol (p.102)
What reaction is catalyzed by Fructose-1,6-bisphosphatase and where does the reaction occur?
Fructose-1-6-bisphosphate –> fructose-6-P. Reaction occurs in the cytosol (p.102)
What reaction is catalyzed by Glucose-6-phosphatase and where does the reaction occur?
Glucose 6-Phosphate –> Glucose. Reaction occurs in the ER (p.102)
What two cofactors are required by Pyruvate carboxylase?
Biotin, ATP (p.102)
What cofactor is required by PEP carboxykinase?
GTP (p.102)
What activates Pyruvate carboxylase?
Acetyl CoA (p.102)
Where does gluconeogenesis primarily occur?
In the liver; enzymes also found in the kidney and intestinal epithelium (p.102)
What results from a deficiency of the key gluconeogenic enzymes?
Hypoglycemia (p.102)
Why can’t muscle participate in gluconeogenesis?
Muscles lack glucose-6-phosphatase (p.102)
What is the product of odd chain fatty acids during metabolism?
Produces propionyl CoA which can directly enter the TCA cycle as succinyl CoA to undergo gluconeogeneis and serve as a source of glucose (p.102)
Why can’t even chain fatty acids produce glucose?
Because they yield two acetyl coA equivalents and no propionyl coA (p.102)
What are the products of the HMP shunt (pentose phosphate pathway)?
Provides a source of NADPH from abundantly available glucose-6-phosphate. Also provides ribose for nucleotide synthesis and glycolytic intermediates (p.103)
What is NADPH used for in metabolism?
NADPH is required for reductive reactions including glutathione reduction inside RBCs (p.103
How can the two phases of the pentose phosphate pathway be classified?
Oxidative and nonoxidative (p.103)
Where does the HMP shunt occur?
In the cytoplasm (p.103)
How much ATP is used and produced in the HMP shunt?
No ATP is used or produced (p.103)
In what tissues does the HMP shunt occur?
Lactating mammary glands, liver, adrenal cortex (sites of fatty acid or steroid synthesis), RBCs (p.103)
Describe the oxidative reaction in the HMP shunt.
Glucose-6-phosphate is converted to 2NADPH and Ribulose-5-P by glucose-6-P dehydrogenase. This is the rate limiting step (p.103)
Is the oxidative reaction of the HMP shunt reversible or irreversible?
Irreversible (p.103)
