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21 Cards in this Set
- Front
- Back
Describe intestinal peptide absorption.
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Digestion
Luminal phase: large proteins broken down to oligopeptides via endo and exopeptidases
Membranous phase: peptidases on brush border hydrolyze further to AAs
Absorption
- AAs (in L-isomer form) can be transported by AA carriers - Di and tripeptides can be absorbed (with protons) by peptide transporters (Pept1, Pept2) and then hydrolyzed intracellularly - Na/H exchange on apical surface
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How are colustrum IgG proteins absorbed in neonates? |
Via pinocytosis. Within 48 hours after birth. |
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Why should you be careful about raw soybeans? |
They contain trypsin inhibitors. Inactivated by heat. |
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What are the different classifications of amino acids? |
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Where are aromatic amino acids mostly used? |
Metabolized in the liver for energy and biosynthesis. Aromatic AAs: Phe, Tyr, Trp |
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Where are branched chain amino acids mostly found? |
In the systemic circulation, where they are taken up and metabolized by muscle via BCAA transaminase. BCAAs: Ile, Leu, Lys, Val |
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What amino acid is preferred by intestinal cells? |
Intestinal cells prefer to oxidize glutamine and asparagine for energy. (This releases alanine, CO2, NH4 and citrulline) |
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What does the kidney use for gluconeogenesis? |
Glutamine |
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What enzymes play a key role in amino acid biosynthesis? |
- Glutamate dehydrogenase - Glutamine synthase (reverse: glutaminase) - Amino transferase |
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What is the glutamate dehydrogenase reaction? |
Deamination
- Key function is to find a way to deal with excess nitrogen!
- Converts glutamate to alpha-ketoglutarate OR VICE VERSA - Ammonia is produced - Higher animals are deficient in alpha-KG (a ketoacid) so they need alpha amino groups in their diet - Animals also can't efficiently deal with excess NH3
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What is the transaminase reaction of AA biosynthesis? |
- Equilibrium reaction that depends on the concentration of AAs - AAs deaminated or ketoacids aminated - IE alphaKG to glutamate, pyruvate to alanine, oxaloacetate to aspartate - critical reaction for metabolic N economy - excess aminogroups could taken care of by feeding ketoacids, such as in the event of liver/renal failure |
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Describe protein digestion in a ruminant. |
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What is the limitation of microbial protein synthesis in the rumen? |
Having enough readily fermentable carbs and ammonia |
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What substrates do microbes need to synthesize proteins? |
- Ammonia (from NPN) - Keto acids (VFAs?) - Energy from CHO |
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How is urea made in the liver? |
- Urea is made from excess rumen ammonia or AA deamination
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What is the rate limiting enzyme in urea synthesis? |
Arginase |
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What happens to urea in ruminants? |
30% excreted in urine 70% recycled through saliva or rumen wall (UT: urea transporter) |
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What happens when there is too much urea fed with low quality forages? |
There is an imbalance between ammonia and carbon availability for the microbes to make protein. Therefore ammonia is absorbed into the blood stream!
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Signs of urea (ammonia) toxicity |
- Rapid, labored breathing - Tremors, incoordination, tetany, recumbency - Occur 20-30 mins after urea ingestion |
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What is the mechanism of urea/ammonia toxicity? |
Too much ammonia increases the rumen pH. This shifts NH4 to more NH3. NH3 is absorbed into the blood more than NH4+.
The liver is overwhelmed and can't convert it all to urea. Therefore it accumulates in the blood, which is toxic. |
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3 treatments for urea toxicity |
1. 5% acetic acid oral drench 2. Cold water drench 3. Rapid rumen evacuation |
