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MBOD Week 13 > Protein Digestion and Amino Acid Absorption > Flashcards

Protein Digestion and Amino Acid Absorption Flashcards

1
Q

What route do amino acids take to get from the enterocyte to the liver?

A

Hepatic Portal Vein

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2
Q

What are the 4 possible fates of an amino acid on entering a cell?

A
  1. Synthesized into Proteins
  2. Nitrogen Containing compounds (purines, pyrimidines)
  3. Energy
  4. Fatty Acids (storage) [Not much in Peripheral Tissues]
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3
Q

How much protein does the average person consume?

- % of american Diet

A

~80 - 100g of protein per day

  • 15% of American diet
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4
Q

What is the difference between essential and non-essential amino acids?
- Which are required in the diet

A

Essential AAs - ones your body can NOT synthesize
* Required in your diet

Non-essention AAs - your body can synthesize these
- Not required in diet

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5
Q

What is the caveat to the hard line between essential and non-essential amino acids?

A

Cys and Tyr can be made from Met and Phe (both essential), thus while Cys and Tyr are Not essential they rely on essential precursors

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6
Q

What amino acid is sometimes required under growth conditions?

A

Arginine

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7
Q

What is the difference in high quality and low quality protein?
- Sources

A

High quality protein contains all essential amino acids in adequate amounts
- e.g. Animal Protein (milk, egg, meat)

Low quality protein is low in one or more essential amino acids
- e.g. Plant protein

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8
Q

T or F: mixtures of low quality protein can be combined so that adequate nutrition is received

A

True

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9
Q

T or F: most of the protein we eat every day comes from what we ingest (exogenous protein)

A

False, Most protein we use is Endogenous Protein (300-600 g) compared to 80-100 g ingest

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10
Q

Where does endogenous protein come from?

A

Protein Turnover in the body

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11
Q

Where do the precursors for amino acid synthesis come from?

A
  • Glycolysis

- TCA cycle intermediates

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12
Q

What is positive nitrogen balance?

- Observed when?

A

Dietary N > Excreted N

- Growth (Childhood and pregnancy)

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13
Q

What is nitrogen balance?

- Observed when?

A

Dietary N = Excreted N

- Normal Healthy Adult

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14
Q

What is negative nitrogen balance?

- Observed when?

A

Dietary N

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15
Q

Kwashiokor

  • causes
  • symptoms
A
  • Deficiency of Protein in a Diet that is Adequate in calories
  • More body proteins get broken down to try to access the essential amino acids tied up in them

Symptoms:

  1. Muscle Wasting
  2. Decreased Concentration of Plasma Proteins
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16
Q

Why are plasma proteins greatly affected in diseases like kwashiokor?
- symptoms of low plasma proteins

A
  • Liver makes plasma proteins
  • Since hepatic portal distributes to liver, its responsible for distributing Amino Acids
  • After distributing Amino Acids its only left with a few that it can turn into serum proteins

**Symptoms = swelling of tissues (stomach usually) because the osmotic pressure is not high enough in blood to draw fluids out of tissues

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17
Q

T or F: Insufficiency of even one essential amino acid can be a major problem

A

True

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18
Q

Where does protein breakdown begin?

  • substances that facilitate this
  • how?
A

Proteolysis in the stomach by:
1. HCl - acidic conditions denatures proteins making them more accessible by proteases

  1. Pepsin - protease
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19
Q

Zymogens

  • what are they?
  • How do they work?
  • Processes that use them
A
  • (aka proenzymes), the are INACTIVE precursors of functional proteins
  • Some conformational change needed to become active
  • Dietary Protein digestion and blood clotting uses zymogens
20
Q

What activates pepsinogen to its active form of pepsin?

A
  • Acidic conditions from HCl causes conformational change

- Protein undergoes AUTOCLEAVAGE to make pepsin (active)

21
Q

T or F: Pepsin is denatured at the pH of the stomach

A

False, that would be dumb

22
Q

Why do processes such as protein degradation and blood clotting use zymogens?

A
  • If protein was active before being released into the appropriate environment, it would destroy proteins in its own cell
23
Q

What is the next phase after stomach acid and enzymes have acted on proteins?

A
  • They are acted on by pancreatic protein
24
Q

What are the 3 pancreatic proteolytic enzymes and their zymogens we have to Know?
- What activates them?

A
  1. Pepsinogen —> Pepsin, via H+
  2. Trypsinogen —-> Trypsin, via Enteropeptidase
  3. Chymotrypsinogejn —> Chymotrypsin, via Trypsin
25
Q

What is special about trypsin?

A

It activates all other digestive proteases

26
Q

Why is their an inhibitor of typisin made in the pancreas?

A

In case the zymogen gets acitivated by accident there is back up system to prevent it from degrading cellular proteins.

27
Q

Why are there so many different proteases?

A
  1. Different Specificities

2. We need to get to single amino acids

28
Q

Why do people with cystic fibrosis sometimes have low serum albumin?

A
  • Dried out pancreatic Ducts prevent proteases from getting to intestines
  • Without proteins being broken down amino acids can’t be absorbed and used for protein synthesis
29
Q

Describe the movement of amino acids from intestinal lumen to peripheral tissue.

A
  1. Amino acids absorbed in intestinal lumen
  2. Transport from lumen to intestinal cell
  3. Hepatic portal vein
  4. From liver into blood
  5. Muscle and Peripheral tissue
30
Q

How are amino acids transported in from the intestinal lumen and then into the hepatic vein tributaries.

A
  1. Na+ - dependent active transport by carriers (secondary active transport)
    - From INTESTINAL LUMEN to CELL
  2. Facilitated Transport (passive transport)
    - from CELL to HEPATIC VEIN
31
Q

How are amino acids transferred from the blood into non-liver cells?

A
  • Principally, Na+ dependent active cotransporters
  • some facilitated transport

**Need the Na+ secondary active transporters because amino acid concentration is higher in the cell than in free fluids so it won’t just move down a gradient

32
Q

T or F: most amino acids can be transported by more than one transporter

A

True

33
Q

Hartnup Disease

  • symptoms
  • causes
A

Symptoms (consistent with pellagra):

  • Photosensitive Rash
  • Ataxia
  • Neuropsychiatric Symptoms

Cause
*Inability of intestine or Kidney Epithelium to absorb NEUTRAL or AROMATIC AMINO ACIDS

34
Q

Why would someone with Hartnups have hyperaminoaciduria?

A
  • Amino acids are reabsorbed in the kidney so you just pee them out
35
Q

Which causes most of the symptoms associated with Hartnups, intestinal and renal malabsorption?

A

Intestinal

36
Q

What is the treatment of Hartnup disease?

- why this?

A
  • Oral Niacin

- Its symptoms result from insufficiency in niacin which can be derived from Trp (TRP NOT ABS. IN DISEASE)

37
Q

Why would you still expect a patient with Hartnup’s who is treated with niacin to still have hyperaminoaciduria?

A
  • Niacin doesn’t fix the transporters, it only prevents deficiency.
38
Q

What is Cystine?

A

Cysteine-Cysteine disulfide bond

39
Q

What disease results from inability of intestine and/or kidney to absorb CYSTINE and basic amino acids?
-signs and symptoms

A

Cystinuria

  • Lots of kidney stones
  • hyperaminoaciduria (high cystine)
40
Q

Why are high Cystine levels a bigger concern in Cystinuria than other amino acids?

A
  • Cystine is insoluble and can generate kidney stones that block the ureter
41
Q

Why would you want increase the pH of urine and fluid intake for someone with Cystinuria?

A
  • Increase in pH will deceaes stones by providing less oxidative conditions
  • Increase in fluid intake decreases the concentration of cystine thus reducing the likelyhood of crystalizaiton
42
Q

Would changing the diet of someone with Cystinuria be affective?

A

Not really, cysteine is derived from methionine so you would need to remove both from the diet to prevent the condition, this would be extremely difficult.

43
Q

Name of Defective transporter in Cystinuria?

- is this disease genetic?

A

membrane transport protein (Bº+)

- Autosomal Recessive

44
Q

Is Kwashiokor disease genetic?

A

No

45
Q

Name of Defective transporter in Hartnup Disease?

- Is this disease genetic?

A

membrane transport protein (Bº)

- Autosomal Recessive

MBOD Week 13 (7 decks)

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