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GI > Wk1 Protein and Lipids > Flashcards

Wk1 Protein and Lipids Flashcards

1
Q

Pepsinogen –> ____?____ –> Pepsin

A

H+

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2
Q

Trypsinogen > ? > Trypsin

A

Enteropepsidase

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3
Q

Chymotrypsinogen > ? > Chymotrypsin

A

trypsin

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4
Q

Proelastase > ? > Elastase

A

trypsin

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5
Q

Procarboxypeptidases > ? > carboxypeptidases

A

trypsin

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6
Q

Exo vs Endo peptidases?

A

Exo – cleave bonds on the end of peptide chains

Endo – cleave bonds within peptide chains

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7
Q

Why do CF patients have trouble absorbing protein?

A

Blockage of pancreatic duct

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8
Q

How do AA get from lumen into cells?

A

Na+ symporter

**Na conc gradient generated by Na/K ATPase

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9
Q

How do AAs get from epithelial cells into blood?

A

Facilitated transport

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10
Q

Transporter for tryptophan

A

Bo aka SLC6A9

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11
Q

What happens if pt is SLC6A9 deficient?

A

Hartnup disease

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12
Q

What are the three hallmark sx of Hartnup disease?

A
  1. Dementia
  2. Dermatitis
  3. Diarrhea
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13
Q

Hartnup disease causes pellagra d/t lack of production of what?

A

niacin

without SLC6A9 can’t absorb tryptophan to synthesize niacin

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14
Q

Niacin is an important component of which molecules:

A

NADH

NADPH

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15
Q

Mutation of SLC7A9 (Bo+) or causes?

A

cystinuria

**loss of basic AA (Arg, Lys, His)

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16
Q

What does cystinuria cause?

A

kidney stones

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17
Q

Two transporter mutation that cause cystinuria?

A
  1. SLC7A9 (Bo+)

2. SLC3A1 (rBAT)

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18
Q

Route for AA absorption but not important for majority of dietary AA uptake?

A

rx with glutathione via gama-glutamyl transpepsidase

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19
Q

4 fates of AAs once they are in the cell:

A
  1. Protein synth
  2. N-containing compounds
  3. Urea cycle
  4. C for TCA cycle
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20
Q

mTORC1?

A

activates protein synthesis and inhibits autophagy

21
Q

ACC ?

A

activiates lipid metabolism

22
Q

AMPK ?

A

inhibits mTORC1 and ACC

promotes autophagy

23
Q

Protein deficiency with normal calorie intake?

A

kwashiorkor

24
Q

PLP

3 jobs in AA metabolism?

A
  1. transaminations
  2. deaminations
  3. carbon chain transfers
25
Q

PLP deficiency causes?

A

seizures

diarrhea

anemia

EEG abnormalities

26
Q

FH4

Job in AA metabolism?

A

one carbon transfers

27
Q

FH4 deficiency causes what?

A

megaloblastic anemia

28
Q

BH4

Job in AA metabolism?

A

ring hydroxylations

29
Q

BH4 deficiency causes what?

A

seizures

developmental delays

30
Q

Two hormones that promote secretion of bile and lipase:

A

secretin

cholecystokinin

31
Q

Triacylglycerol + pancreatic lipase –> ?

A

2 fatty acids + 2-monoacylglycerol

32
Q

What does PLA-2 do?

Where does it come from?

A

cuts the #2 fatty acid from phospholipids

pancreas

33
Q

Breaks down big balls of fat into little balls of fat:

A

bile salts

34
Q

What happens to fatty acids once in the gut epithelial cells?

A

Converted back to TAG

Packaged as nascent chylomicrons and dumped into lymphatics

35
Q

Apoprotein of nascent chylomicrons:

Where do they get this?

A

ApoB-48

From RER in epithelial cells before going to lymph

36
Q

How do you get ApoB-48 from same DNA as ApoB-100?

A

RNA editing

37
Q

What do nascent chylomicrons get once they enter the blood?

Where do they get it?

A

ApoCII

ApoE

–from HDL

38
Q

What activates LPL to cut FAs from chylomicrons?

39
Q

What happens to chylomicron remnants in the liver?

A

repackaged with ApoB-100 as VLDL

40
Q

What do adipocytes need to store FAs?

A

glycerol 3-phosphate backbones from glycolysis

**so they can only store in fed state

41
Q

Fat transport molecules from largest to smallest:

A

Chylomicron (huge by comparison)

VLDL

ILDL

LDL

HDL

42
Q

Transfer DIETARY fat from gut to tissue:

A

chylomicrons

43
Q

Transfer fat produced by dietary CARBS to tissue:

44
Q

Where do VLDL come from:

45
Q

In charge of cholesterol and apoprotein homeostasis:

46
Q

Source of HDL:

A

liver and intestine

47
Q

ApoB48
ApoCII
ApoE

Whats is it?

A

Chylomicron

48
Q

ApoB100
ApoCII
ApoE

What is it?

A

VLDL

or ILDL

49
Q

ApoB100

What is it?

GI (46 decks)

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