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GI Week 1 - WLB > Proteins & Lipids - Skildum > Flashcards

Proteins & Lipids - Skildum Flashcards

1
Q

What are the general steps of protein digestion?

A
  1. Mechanical
  2. Low pH denatures proteins; activates pepsinogen
  3. Enzymatic digestion: Lumenal proteases digest to tripeptides, dipeptides, and amino acids
  4. Tripeptides, dipeptides and amino aicds are transported into the intestinal epithelial cell
  5. Intracellular peptidases digest tri- and dipeptides to amino acids
  6. Amino acids are transported into the blood
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2
Q

What is protein malnutrition called?

A

Kwashiorkor

(adequate calories, but deficient in protein)

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3
Q

What is the oxidized form of cysteine called?

A

Cystine

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4
Q

Pepsinogen becomes what active enzyme via activation by what?

A

Pepsinogen => H+ => Pepsin

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5
Q

Trypsinogen becomes what active enzyme via activation by what?

A

Trypsinogen => Enteropeptidase => Trypsin

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6
Q

Chymotrypsinogen becomes what active enzyme via activation by what?

A

Chymotrypsinogen => Trypsin => Chymotrypsin

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7
Q

Proelastase becomes what active enzyme via activation by what?

A

Proelastase =>Trypsin => Elastase

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8
Q

Procarboxypeptidases becomes what active enzyme via activation by what?

A

Procarboxypeptidases => Trypsin => Carboxypeptidases

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9
Q

What is the difference between Endopeptidases and Exopeptidases?

A
  • Endopeptidases cleave peptide bonds within a chain. Their specificity is determined by the side chain of the carbonyl containing amino acid.
    • Trypsin, e.g., cuts peptide bonds in which the carbonyl is provided by arginine or lysine.
  • Exopeptidases cut single amino acids from the ends of peptide chains. (e.g. carboxypeptidase)
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10
Q

Why is protease secretion deficient in patients with cystic fibrosis?

A
  • In patients with cystic fibrosis, secretion of proteases is deficient because of blockage of the pancreatic duct.
    • Malabsorption of protein an other nutrients can result.
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11
Q

How are proteins absorbed in the gut?

A
  • Amino acids are transported across intestinal epithelial cells using secondary active tranport.
    • via Na+/AA symporter that uses the concentration gradient set up by the Na+/K+ ATPase
    • enter the portal vein circulation via facilitated transporter
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12
Q

Inherited mutations in what transporter result in Hartnup disease?

A
  • SLC6A9 transporter (B0)
    • not able to transport dietary tryptophan into their cells
    • specific for Zwitterionic amino acid substrates
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13
Q

What symptom results in Hartnup disease? Why?

A
  • This condition results in the symptoms of pellagra
    • because tryptophan is not absorbed or resorbed and can not be used to synthesize niacin.
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14
Q

What are the symptoms specific to pellegra?

A
  • High sensitivity to sunlight
  • Aggression
  • Dermatitis
  • Alopecia (hair loss)
  • Edema (swelling)
  • Smooth, beefy red glossitis (tongue inflammation)
  • Red skin lesions
  • Insomnia
  • Weakness
  • Mental confusion
  • Ataxia (lack of coordination)
  • Paralysis of extremities
  • Peripheral neuritis (nerve damage)
  • Diarrhea
  • Dilated cardiomyopathy (enlarged, weakened heart)
  • Eventually dementia
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15
Q

Inherited mutations in what transporter result in Cystinuria?

A

SLC7A9 (B0+) or SLC3A1 (rBAT)

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16
Q

What major problem develops in Cystinuria?

A

Patients develop kidney stones.

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17
Q

How can amino acids be transported across cellular membranes?

A
  • Reacting with glutathione!
    • This pathway is important for glutathione synthesis, but not a major contributor to the transport of dietary amino acids.
    • AA displaces glutamate in the glutathione molecule
    • release Cysteine and Glycine and transported AA intracellularly
    • glutathione regenerates to transport next AA
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18
Q

What are the amino acids used for once absorbed?

A
  • Synthesize proteins
  • Donate nitrogens to production of neurotransmitters, nucleotides, hormones, and other nitrogen-containing compound synthesis
  • Split into carbon and oxidized (for energy)
    • Nitrogen gets eliminated (in Urea cycle)
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19
Q

What are the three sources of the intracellular amino acid pool?

A
  • Extracellular amino acids
  • Protein degradation
  • de novo synthesis from glycolysis or TCA cycle intermediates
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20
Q

How is the balance between protein synthesis and degradation controlled?

A
  • sensitive to the metabolic state in the cell:
    • insulin promotes protein synthesis
    • AMPKinase inhibits protein synthesis and promotes autophagy (breakdown proteins)
    • mTORC1 complex activates protein synthesis and inhibits autophagy
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21
Q

What key cofactor in amino acid metabolism is important for transaminations, deaminations, and carbon chain transfers and can result in seizures diarrhea, anemia, and EEG abnormalities if deficiency is present?

A

PLP

22
Q

What key cofactor in amino acid metabolism is important for one carbon transfers and can result in megaloblastic anemia if deficiency of it is present?

A

Tetrahydrofolate (FH4)

23
Q

What key cofactor in amino acid metabolism is important for ring hydroxylations (e.g. Phe => Tyr) and can result in seizures and developmental delays if deficiency is present?

A

Tetrahydrobiopterin (BH4)

24
Q

What is the most calorically dense food?

A

Fat

25
Q

What particle functions to promote cholesterol homeostasis?

A
  • High density lipoprotein
    • perform reverse cholesterol transport
    • take excess cholesterol from tissues back to the liver
26
Q

What lipoprotein activates an extracellular lipase in capillary beds?

A

ApoCii

27
Q

What particle functions to distribute dietary fat to tissues?

A
  • Chylomicrons transfer dietary fat from gut → tissues
    • Dietary fat: triacylglycerol, phospholipids, cholesterol esters
28
Q

What do we do with fatty acids in the body?

A
  • Oxidation => CO2 + H2O
  • Triacylglycerol (adipose tissue stores)
  • Phospholipids and sphingolipids (signaling molecules like arachodonic acid)
29
Q

What two arachidonic acid by-products can cause Lower Esophageal Sphincter contraction?

A
  • Prostaglandins
  • Thromboxanes
30
Q

What are the basic steps of fat digestion?

A
  1. Mechanical digest in mouth and stomach
  2. Enzymatic digestion in the Small Intestines by bile salts from the gallbladder and lipases from the pancreas
  3. Fatty acids packaged into chylomicrons for transport to the blood
31
Q

What two hormones promote secretion of bile and lipases into the lumen of the gut?

A

secretin and cholecystokinin (CCK)

32
Q

Why does malabsorption of lipids occur in patients with cystic fibrosis?

A

secretion of lipases is deficient

because of blockage of the pancreatic duct

33
Q

What are the products of triacylglycerol reacted with pancreatic lipase?

A
  • Two fatty acids
  • 2-monoacylglycerol
34
Q

What is the typical digestion of long chain fatty acids?

A
  • Triacylglycerol + Bile salts => Triacylglycerol in Micelles
  • Micelles + Pancreatic Lipase => 2 FA’s + 2-monoacylglycerol
  • 2 FA’s + 2-monoacylglycerol => uptake by gut epithelial cells
  • Recreate triacylglycerol => package into chylomicrons
  • Chylomicrons => lymphatic transport
  • Lymph => Chylomicrons enter blood
35
Q

What is different about the digestion of short and medium chain fatty acids compaired to long ones?

A
  • Triacylglycerol + Bile salts => Triacylglycerol in Micelles
  • Micelles + Pancreatic Lipase => 2 FA’s + 2-monoacylglycerol
  • 2 FA’s + 2-monoacylglycerol => uptake by gut epithelial cells
  • BUT short and medium chain FA’s => DIRECTLY TO PORTAL BLOOD SYSTEM!
    • (don’t have to be packaged into chylomicrons and navigate lymph to enter blood)
36
Q

How is fat consumed as cholesterol esters?

A
  • by Pancreatic Cholesterol Esterase
    • products =
      • Cholesterol
      • free fatty acid
37
Q

How is fat consumed as phospholipids broken down?

A
  • by Pancreatic Phospholipase A2
    • products =
      • Lysophospholipid
      • free fatty acid
38
Q

How is fat packaged into a nascent chylomicron?

A
  • (Reform triacylglyceride => SER) + (ApoB48 => RER)
  • ===> GOLGI Complex forms Nascent chylomicrons
    • ***only for dietary fat
39
Q

How is ApoB48 formed?

A
  • RNA editing produces ApoB-48 in intestinal epithelial cells.
    • ***The unedited transcript produces full length ApoB-100 in HEPATOCYTES.
40
Q

What happens to the Nascent Chylomicrons after they leave the intestines and enter the blood?

A

They receive ApoCII and ApoE from high density lipoprotein (HDL).

41
Q

What is HDL’s function?

A
  • maintain cholesterol and apoprotein homeostasis
  • go out and make sure that the other particles have what they need
  • can perform reverse cholesterol transport if something has too much cholesterol
42
Q

What does ApoCii do?

A
  • Allow chylomicrons to deliver cholesterol to the appropriate tissues.
    • interacts with LPL receptor to signal release of fatty acid and glycerol, so that it can be taken up by adjacent tissue (either muscle or adipose)
43
Q

What is LPL?

A
  • Lipoprotein lipase (LPL) is an extracellular lipase in the capillary beds of muscle and adipose tissue.
    • It is activated by ApoCii.
44
Q

How is VLDL different from chylomicrons?

A
  • Similar function:
    • deliver fatty acid fuels to the tissue of the body
    • BUT only delivers ***non-dietary fat/synthesized fat!
    • Fatty acids and cholesterol taken up by the liver from chylomicron remnants can be repackaged with ApoB100 as very low density lipoprotein (VLDL).
  • Made in liver: from RER + Secretory Vesicle in golgi
45
Q

How does VLDL drop off contents to adipose tissue?

A

ApoCii on VLDL interacts with LPL receptor => triggers release of fatty acid and glycerol

46
Q

How does Adipose store fatty acids?

A
  • Adipose can only store fatty acids as triacylglycerol in the fed state
    • because the glycerol 3-phosphate backbone can only be produced by glycolysis in adipocytes.
47
Q

What particle functions to deliver dietary fat to tissues?

A

Chylomicrons

48
Q

What particle functions to distribute fat synthesized from carbs to tissues?

A

VLDL

49
Q

The apoproteins ApoB100 and ApoB48 are encoded on the same gene. The different apoproteins are produced through ____________________.

  • A. alternative exon splicing
  • B. alternative promoter utilization
  • C. proteolytic cleavage
  • D. RNA editing
  • E. post-translational modification
A

D. RNA editing

50
Q

What particle functions to distribute cholesterol synthesized in the liver to tissues?

A

Low density lipoprotein

GI Week 1 - WLB (11 decks)

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