IAS14

Question 1

AA digestion in stomach

Answer 1

pepsinogen secreted by stomach chief cell
self-cleaves & activates to form pepsin under low pH (HCl), hydrolyses AA

Question 2

AA digestion in intestine

Answer 2

pancreas secretes zymogens (trypsinogen, etc.) -> enteropeptidase cleaves trypsinogen to form trypsin -> trypsin cleaves zymogens to form functioning proteins i.e. endopeptidases, e.g. chemotrypsin, elastase, carboxypeptidase
endopeptidases cleave peptides to form di/tripeptide
exopeptidase secreted by enterocytes & sit on brush border for digestion of short chain AA
pH rises due to bicarbonate -> start cleaving

Question 3

AA absorption by enterocyte

Answer 3

take in AA, dipep, tripep
Na+ dependent carrier takes in AA along with Na -> Na+ pumped out for K+ by Na+/K+ ATPase pump
peptides cleaved to form AA
basolateral membrane: only free AA carried by facilitated transporter out down conc. gradient (secondary active transport)

Question 4

polypeptide entering blood & clinical relevance

Answer 4

pinocytosis or slipping between enterocytes
can cause allergy to protein containing food in infants

Question 5

endogenous source of proteins

Answer 5

protein turnover i.e. protein degradation in 2 methods: ubiquitin-proteasome, autophagy

Question 6

ubiquitin proteasome method (OPTIONAL)

Answer 6

protein covalently linked to ubiquitin -> interact w/ proteasome -> degrade protein to small peptides using ATP -> ubiquitin recycled

Question 7

autophagy of proteins (OPTIONAL)

Answer 7

unwanted IC components surrounded by membranes fuse with lysosome -> cathepsin cleaves proteins into AA

Question 8

amino acid pool

Answer 8

free AA enter or leave AA pool
+: exogenous / endogenous AA sources, AA synthesis in body w/ N & glucose supply
-: new protein synthesis, biomolecule synthesis, AA degradation into N, AA used as fuel or through GNG, transamination & carbon skeleton removed for GNG

Question 9

transamination

Answer 9

in liver, amino group transferred from AA to alpha keto acid, original AA -> alpha keto acid
coupled w/ AA transaminase & cofactors

Question 10

fate of protein degradation & transamination products

Answer 10

C skeletons converted to glucose or TAG
TAG packaged, secreted from liver by VLDL -> long term fuel storage
glucose stored in glycogen or released to blood
alpha keto acid enter TCAC at diff. points as energy sources when glucose unavail.
N: disposed of

Question 11

urea disposal & carriers

Answer 11

as equal amts of ingested & excreted N every day, waste product from AA -> NH3 sources & must be disposed of
all peripheral cells have N disposal -> transfer to liver for disposal as urea using Ala & Gln (major N carriers)
muscle, intestinal, kidney cells use Ala for carrier
muscle, lung, neuron use Gln for carrier

Question 12

NH3 toxicity

Answer 12

hyperammonemia, neurotoxic to CNS
can occur in disorders of urea cycle

Question 13

deamination Rx e.g.

Answer 13

amino group from Gln or other not taken up by alpha keto acid -> NH4+ & AKA (incl. pyruvate) forms

Question 14

glucose-alanine cycle

Answer 14

during exercise or fasting when muscle use blood-borne glucose
AA degradation -> pyruvate gains N from Glu -> Ala -> travels to liver -> pyruvate -> glucose via GNG -> to peripheral tissue
i.e. backbone of Ala make glucose, amino group fed to urea cycle

Question 15

alanine -> pyruvate Rx

Answer 15

AKG -> Glu, 2 fates
1. -> transaminated to AKG, OAA forming Asp -> enter urea cycle
2. -> deaminated to AKG by directly forming NH4+

Question 16

glutamine in N disposal

Answer 16

inter-organ amino exchange in fasting -> AA use for fuel or biosynthesis of compounds / proteins
AKG -> Glu -> Gln (by accepting 2x NH4) -> travel in blood to liver -> AKG -> NH4 released into urea cycle

Question 17

urea cycle

Answer 17

in liver hepatocytes
converts harmful NH3 into harmless urea which can be excreted, maintain N balance & get rid of toxic NH3
takes 1x NH4 from deamination of glutamate, 1x NH4 from Asp

Question 18

excess AA fate in fed state

Answer 18

make proteins in liver or exported to peripheral cells
biosynth. of N-containing compounds
degraded to pyruvate (TCAC) & ammonia (urea cycle) –> energy storage in lipid & glycogen

Question 19

AA metabolism in fasting state

Answer 19

net degradation of skeletal muscle proteins -> AA used to provide energy via GNG or KB production -> N deaminated by transport by Ala & Gln