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MONOGASTRIC GI > 6.6 – Utilization and Excretion of AA and N > Flashcards

6.6 – Utilization and Excretion of AA and N Flashcards

1
Q

What % of AA are catabolized in entereocytes or by luminal bacteria?

A

-25-95%

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2
Q

What % of AA, di- and tri-peptides are absorbed by the portal vein?

A

-5-75%
>metabolized in liver (and other tissues)

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3
Q

What happens at high levels of ammonia/ammonium?

A

-toxic
>liver converts it into urea
*muscle tissue is UNABLE to dispose of ammonium ions

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4
Q

What happens when pH is low for the ammonia/ammonium equilibrium (pKa=9.25)?

A

-shifts to the right: favours ammonium (NH4+)
Ex. pH=7.4, 98% will exist as ammonium
*uncharged ammonia moves easily across biological membranes

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5
Q

How much of the urea synthesized in the liver reaches the GIT by diffusion from blood?

A

-25%

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6
Q

What happens to urea in the colon?

A

-bacterial ureases converts it to NH3 (ammonia)

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7
Q

What is the expected concentration of ammonia in the portal vein?

A

-250uM

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8
Q

What is the expected concentration of ammonia in the hepatic vein?

A

-30uM

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9
Q

Pyruvate into alanine in muscle and then to the liver:

A

-alanine transaminase (ALT)
-L-alanine is shuttled to liver and deaminated
>forms pyruvate again (some goes back to glucose
>NH2 that was released is used to synthesize urea
*alanine is a safe way to transfer N

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10
Q

Glucose-alanine cycle: following a meal (fed state)

A

-splanchnic tissues release AA
-peripheral muscle extract AA (especially BCAA)

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11
Q

Cahilii cycle: post-absorptive state (fasted state):

A

-free AA (especially alanine and glutamine) are released from muscle into circulation
>alanine=key gluconeogenic AA
>NH2 is converted to urea

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12
Q

What happens to extracellular and intracellular ammonia?

A

-liver converts it into urea
*high levels of ammonia=toxic

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13
Q

Urea:

A

-water soluble (easily passed in urine)
-non-toxic
-synthesized in liver (requires energy)
-not ionized at physiological pH

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14
Q

Other species use different compounds to dispose of excess N:

A

-fish: make ammonia and flush it out using water
-birds: excrete uric acids (they don’t have urine)

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15
Q

What are the steps of the biosynthesis of urea?

A
  1. Transamination (need vitamin B6)
  2. Oxidative deamination of glutamate
  3. Ammonia transport
  4. Urea cycle
    *enzymes of urea cycle are increased during STARVATION
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16
Q

Transamination (biosynthesis of urea)

A

-freely reversible
-pyridoxal phosphate (derivative of Vitamin B6)
*all N from AA can undergo it and be concentrated as L- alanine and L-glutamate

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17
Q

Pyridoxal phosphate:

A

-derivative of Vitamin B6
-co-enzyme of all aminotransferases

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18
Q

L-glutamate from transamination:

A

-utilized by body to transport NH3
*only AA that undergoes oxidative deamination in mammalian tissues

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19
Q

Oxidative deamination of glutamate (biosynthesis of urea):

A

-transfer N to alpha-ketoglutarate by GDH
-freely reversible
-use either NAD+ or NADP+
-releases N as NH3
-occurs in liver

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20
Q

GDH:

A

-L-glutamate dehydrogenase
-in the liver
-transfers N to alpha-ketoglutarate

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21
Q

What inhibits liver GDH?

A

-ATP
-GTP
-NADH

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22
Q

What activates liver GDH?

A

-ADP

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23
Q

What can ammonia be produced by?

A

-enteric bacteria
-extra-hepatic tissues

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24
Q

Ammonia transport (biosynthesis of urea):

A

-glutamate synthetase
-glutamine sequesters ammonia=non-toxic form
-glutaminase

25
Q

Glutamate synthetase:

A

-“fixes” NH4+ as glutamine
>strongly favoured by reaction of ATP to ATP+P

26
Q

Where is glutamate synthetase ubiquitously present?

A

-liver
-muscle
-brain
-adipose
-lung

27
Q

Glutaminase:

A

-irreversibly get glutamate and NH4 formation
-in hepatocytes

28
Q

What is the rate limiting step of the urea cycle?

A

-condensation of CO2, ammonia and ATP=carbomyl phosphate
-catalyzed by carbomyl phosphate synthase I
-occurs in mitochondria

29
Q

N-aceylglutamate:

A

-allosteric=changes shape of molecules to allow the reaction to proceed
*upregulates CPS1

30
Q

CPS1:

A

-carbamoyl phosphate synthase 1

31
Q

What conditions favour high rates of urea synthesis?

A

-substrate availability, including co-factors
-inadequate intake of arginine (kittens and puppies)
>becomes an essential AA and protein synthesis stops (other proteins become catabolized instead)
-protein intake above optimal (especially imbalanced)
-high levels of glucocorticoids

32
Q

What can decrease urea synthesis?

A

-low protein diets
-low birth-weight neonates
-acute metabolic acidosis
-growth hormone and insulin

33
Q

What can cause hyperammonemia?

A

-sudden consumption of a high protein diet following a period of malnutrition
*could be life threatening

34
Q

Blood (or plasma or milk) urea N:

A

-can indicate renal function and/or liver health
*use MUN to see if you are feeding correct/enough protein in the diet (balance of AA)

35
Q

When does decreased blood urea N occur?

A

-chronic, severe liver disease
-low protein diets
-drugs causing diuresis
-overhydration
-increase protein synthesis

36
Q

When does increased blood urea N occur?

A

-blood loss
-dehydration
-recent high protein meal
-kidney infection or inflammation
-bladder or urethral obstruction

37
Q

How much ATP does it take to make urea from ammonium?

A

-6.5ATP/mol urea
-could be reduced if fumurate goes into TAC cycle
*a lot of energy

38
Q

High protein diet to lose weight:

A

-takes a lot of energy to get rid of the N
*it does work

39
Q

Energy ‘ladder’ from diet:

A

-gross energy (100%) -> lost in feces
-digestible energy: lost in urine and gases
-metabolizable energy: lost in heat increment (significant!)
-net energy (60%)

40
Q

Metabolizable energy:

A

-energy available to the body for maintenance and production (ex. growth)
-some lost during metabolism=heat increment (ex. urea cycle)

41
Q

Net energy:

A

*gold standard
-harder to measure compared to gross and digestible energy
-often just CALCULATED

42
Q

Example: soybean meal and wheat:

A

*diets higher in protein (ex. soybean meal) are overestimated due to more energy being needed for the urea cycle
-decrease the amount of energy that protein can make (to counter how much energy it takes to metabolize it)

43
Q

All urea cycle disorders are characterized by:

A

-hyperammonemia (TOXIC!)
-encephalopathy (brain dysfunction)
-respiratory alkalosis

44
Q

What happens in urea cycle disorders?

A

-accumulation of precursors of urea (ammonia and glutamate)
>severe blockages occurs at first 2 reactions of urea cycle

45
Q

Encephalopathy as a clinical sign:

A

-when exogenous and endogenous sources of ammonium overwhelm the liver,
-the liver is diseased
-urea cycle is broken

46
Q

What are causes of increased ammonium?

A

-too much N
-liver failure for any reasons
-portal system shunt
-urea cycle defects

47
Q

Portal systemic shunt:

A

-blood passes by the liver
-congenital or acquired
-extrahepatic or intrahepatic

48
Q

Decreased uptake of ammonia can be due to:

A

-abnormalities in hepatic blood flow
-hepatic dysfunction
*may result in decreased urea in blood

49
Q

Decreased conversion to urea can be due to:

A

-hepatic dysfunction
-inherited disorders of urea cycle (cats and irish wolfhounds)
-lack of urea cycle intermediates
-organic acidemias

50
Q

Increased production of ammonia can be due to:

A

-excessive growth of urease-producing enzymes in the GIT
>rumen: “urea toxicosis:
>colon: in horses leading to neurological signs

51
Q

Toxicity can be due to?

A

-accidental poisoning with anhydrous ammonia
-urea toxicity in cattle

52
Q

Brain issues with NH4+

A

-blocks channels and transporters
-increased glycolysis=acidosis and lack of energy

53
Q

Uric acid:

A

-used by birds and reptiles to remove ammonia
-weak acid (pKa=5.75)
>at physiological pH=sodium salt (stable)
-low pH=NOT water soluble
-33% N by weight
*can be used by dalmatians

54
Q

What is uric acid formed from?

A
  1. Degradation of purine nucleotides (RNA, DNA)
    >Feed a low purine diet to prevent it
  2. De novo synthesis from bicarbonate and ammonia (birds)
55
Q

What is similar between the uric acid and the urea cycle?

A

-occurs in mitochondria in the liver
-both start with bicarbonate and ammonia
-different intermediate steps

56
Q

What are the ATP requiring reactions for uric acid synthesis?

A

-formation of adenosine or guanosine
-incorporation of ammonia into Gln, Asp, Gly
-formation of N-formyl-tetra-hydrofolate from formate and tetrahydrofolate

57
Q

What is the energy requirement of uric acid synthesis?

A

-18.5-19.5 mol ATP

58
Q

Why do birds still synthesis uric acid even though it cost more energy?

A

-allows birds to maintain higher body T
-conserves water
-maintain low body weight
-scavenges O2=reduces free radicals

59
Q

Dalmatians:

A

-autosomal recessive trait
-missing some transporters to take up urea which shunts it to uric acid=not soluble
>crystals can build up in the bladder and cause problems
*feed a low purine diet

MONOGASTRIC GI (24 decks)

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