Week 4 Amino Acid/Nitrogen Metabolism Flashcards
What are the main precursors of glucose that the carbon skeleton of glucogenic amino acids can be converted into?
pyruvate, oxaloacetate, other intermediates of the TAC
In the fed state, when protein is digested and broken down into amino acids by the small intestine, they are delivered to the _________ where they can be used directly for ___________ synthesis, converted to __________ OR ______ _______, or delivered to other tissues most notably the __________.
When protein is digested and broken down into amino acids by the small intestine, they are delivered to the LIVER where they can be used directly for PROTEIN synthesis, converted to GLUCOSE OR FATTY ACIDS, or delivered to other tissues most notably the MUSCLES.
Note:
-When converted to glucose or fatty acids, those are stored as glycogen and triacylglycerides. This occurs when AA are in excess.
-When delivered to muscles AA’s are used for protein synthesis.
What are the main precursors of fatty acids that carbon skeletons of ketogenic amino acids can be converted to?
acetyl -COA and acetoacetyl CoA.
In the fasted state, most ___________ amino acids will contribute to the production of _______ via the process of ____________ while others will form ATP by going into the _________ cycle.
In the fasted state, most GLUCOGENIC amino acids will contribute to the production of GLUCOSE via the process of GLUCONEOGENESIS while others will form ATP by going into the KREBS cycle.
When in starvation, does the body use ketogenic amino acids?
It certainly can. However, first, it will oxidize fatty acids released from adipose tissue for energy. The whole point of ketogenesis is to preserve proteins so they don’t have to break down.
The transamination step is when an _______ group is transferred to another molecule for eventual excretion so it can free the _-_____ _____ to contribute to metabolic pathways.
The transamination step is when an AMINE group is transferred to another molecule for eventual excretion so it can free the ALPHA-KETO ACID (carbon backbone) to contribute to metabolic pathways.
T/F: In times of starvation, fatty acids and amino acids are used in gluconeogenesis.
False, only amino acids.
AAs can be converted to pyruvate, oxaloacetate (the first bypass step) in gluconeogenesis, as well as PEP (after converted to OAA). **AA can also be turned into acetyl CoA but those will not contribute to gluconeogenesis.
FA: acetyl CoA can never be converted to pyruvate because 1) the reaction of pyruvate to acetyl-coA is irreversible and 2) Acetyl-CoA only provides 2 carbons for the TAC that are eventually lost before becoming OAA.
What happens to excess protein?
It’s excreted, there is no longterm storage for AAs
What are the major sources of ammonia/ammonium?
gut bacteria, transamination, deamination, purine/pyrimidine degradation…
What are the 3 major fates of amino acids?
1) Synthesis of tissue proteins
2) Synthesis of other important constituents (nucleotides, neurotransmitters, heme, etc.)
3) Catabolism and excretion
Describe the two main systems for degrading proteins within the cell.
- Ubiquitin-protease system (UPS) (ATP-dependent) involves tagging protein with ubiquitin and degrading in the proteosome
- Proteases in lysosomes also degrade proteins (ATP-independent)
How can you use amino acids for energy?
Direct carbon skeletons into TCA cycle
In animals, why can fatty acids not be used for glucose production?
2-C Acetyl CoA product of FA oxidation enters TCA cycle, but 2 CO2 come out, so OAA is regenerated but there is no net gain of OAA, which is also used in gluconeogenesis
Pyruvate dehydrogenase catalyzing pyruvate-> acetyl CoA is irreversible, so 2C acetyl CoA not used to regenerate 3C pyruvate
Why do patients with a protein calorie deficiency present with edema and ascites?
In Kwashiorkor, hypoproteinemia, hypoalbuminemia lead to ascites (colloid osmotic pressure reduced, fluid goes to tissue & see edema)
Hepatomegaly from enlarged fatty liver from carbohydrate diet
What role do bacteria play in contributing to hyperammonemia?
Bacterial urease causes NH4+ release in the gut, which can increase its levels in the blood.
In viral hepatitis, why do you see an increase in serum aminotransferases and jaundice?
Increased liver damage causes increased enzymes in serum
Hepatic damage may result in decreased bilirubin conjugation so less is excreted, resulting in jaundice; this is last hepatocyte function to be lost
Why might alcoholism lead to hyperammonemia?
Liver damage can lead to compromised urea cycle and thus the buildup of NH4+.
What is a biochemical and physiological consequence of a genetic defect causing a deficiency in a urea cycle enzyme?
Hyperammonemia; defect in earlier enzymes in cycle may cause more severe form; arginase deficiency (argininemia may be asymptomatic. Ornithine transcarbamylase (OTC) deficiency is most common urea cycle disorder.
What is ornithine transcarbamoylase?
OTC is a urea cycle enzyme that catalyzes the reaction between ornithine and carbamoyl phosphate and thus allows a nitrogen to enter the cycle.
What does a deficiency in OTC do?
A deficiency in OTC causes urea cycle deficiency. Increasing serum ammonia levels result. As an early enzyme in the urea cycle, OTC deficiency may cause a more severe hyperammonemia than other urea cycle enzyme deficiencies.
What macromolecule is used first for energy in starvation?
Glycogen broken down to glucose, released from liver to blood
