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GI Exam 2 > Nutrition > Flashcards

Nutrition Flashcards

1
Q

Main Dietary Carbohydrates

A 
Fructose
Lactose (galactose + glucose)
Sucrose (fructose + glucose)
Amylose (alpha-1,4- bonds)
Amylopectin (alpha-1,6 and 1,4 bonds) --> most similar to glycogen
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2
Q

Dietary Disaccharides

A 
lactose = beta-1,4
sucrose = alpha-1,2
trehalose = alpha-1,1 (mushrooms)
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3
Q

Absorption of fructose and disaccharides

A

unchanged

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4
Q

Absorption of starches

A

1) salivary amylase cuts into smaller chunks

2) pancreatic amylase –> same

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5
Q

Amylase

A

it is a endoglycosidase –> cuts alpha-1,4 bonds in polysaccharides (highest activity in duodenum)
- won’t get free glucose with an endoglycosidase

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6
Q

Disaccharidases of brush border

A
  1. Glucoamylase
  2. Sucrase/Isolmaltase
  3. Trehalase
  4. beta-glycosidase complex
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7
Q

Glucoamylase

A

also called maltase –> exoglycosidase

  • cleaves alpha-1,4 bonds of maltose to 2 glucose off non-reducing ends of starch
  • activity is highest in ileum
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8
Q

Sucrase/Isolmaltase

A
  • complex has 2 extracellular domains with different substrate specificities
    Sucrase cuts sucrose into glucose and fructose
    Isolmaltase cuts alpha-1,6 in isolmaltose
  • activity highest in jejunum
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9
Q

Trehalase

A

only one catalytic site and one substrate = trehalose

Trehalose = 2 glucose bonded through carbon #1

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10
Q

Beta-glycosidase complex

A

its a glycophosphatidylinositol glycan anchored protein with 2 catalytic domains

  • Glucosyl ceramide domain –> cuts glucose and galactose from glucosylceramide
  • Lactase domain –> splits 1,4 bond in lactose into glucose and galactose
  • activity is highest in jejunem
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11
Q

Gaucher’s disease

A

defect in beta-glycosidase in lysosomes (lysosomal storage disease)
If beta-glycosidases are lost in gut –> they just get pooped out

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12
Q

Carbohydrate absorption

A
  1. When carb [ ] is higher in lumen than blood –> facilitated diffusion through gradients created by Na/K channel
  2. When carb [ ] is lower in lumen than blood –> hydrolysis of ATP
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13
Q

Pathology of lactose intolerance

A

without lactase –> bacteria ferment lactose to lactic acid in gut –> water enters the lumen of gut to balance the extra H+ [ ] –> causes watery diarrhea
- 8 oz glass of milk –> 1 L diarrhea

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14
Q

Protein digestion

A
  1. Mechanical
  2. low pH –> denatures, pepsinogen
  3. lumenal proteases digest tripeptides, dipeptides and AA
  4. Tri-, dipeptides and AA transported into cell
  5. Intracellular peptidases digest tri and di peptides into AA
  6. AA are transported into blood
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15
Q

Fate of AA inside cell

A
  1. synthesize protein
  2. synthesize N-containing compounds
  3. TCA cycle –> carbon
  4. Nitrogen –> urea cycle
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16
Q

3 key cofactors for enzymes in AA metabolism

A
  1. PLP –> all AA use this (transaminations, deaminations)
    - seizures, diarrhea, anemia, EEG abnormalities
  2. FH4 –> one carbon transfers
    - megaloblastic anemia
  3. BH4 –> ring hydroxylations
    - seizures, developmental delays
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17
Q

AMP kinase

A

sensor of intracellular energy level

- low energy level –> inhibits ACC (lipid metabolism), and mTORC1 (protein translation)

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18
Q

Ways to get Fatty Acids

A

from diet –> TAG, phospholipids, cholesterol esters

synthesis of FAs from glucose

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19
Q

Uses of Fatty Acids

A

oxidation for energy
storage of TAG (2-way street)
cell membrane synthesis

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20
Q

Biochemical digestion of fats

A

doesn’t start until entering the small intestine –> bile salts from gall bladder

  • bile salts are detergents that mix up fats form micelles
  • lipase from pancreas cleaves TAG into FA and 2-MG
  • absorbed into nascent chylomicrons
  • bile salts recycled through ileum
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21
Q

Pancreatic lipase

A

cuts TAG at #1 and 3 position creating 2 Fatty acids and 2-monoacylglycerol
- pancreas also has PLA-2 which cuts #2 from the triacylglycerol –> not required for digestion

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22
Q

Packaging of FAs for transport

A

FAs and 2-monoacylglycerol are taken up by gut epithelial cells and form chylomicrons
- 6-8 C FAs can be transported without chylomicrons

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23
Q

Cholesterol digestion

A

cholesterol eaten as cholesterol ester –> cholesterol esterase from pancreas cuts off the Fatty Acid to make 1 FA and 1 cholesterol

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24
Q

Phospholipid digestion

A

phospholipid has a FA tail and a polar head group

- phospholipase A2 cuts off FA making 1 FA and a lysophospholipid

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25
Q

What happens to the FAs once absorbed?

A

FAs are re-esterified to glycerol to make TAG in epithelial cells

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26
Q

ApoB-48

A

major apoprotein of chylomicrons from dietary fats

- encoded by same gene that makes ApoB-100

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27
Q

ApoB-100

A

major apoprotein of chylomicrons of fat from liver

  • encoded by B-apoprotein –> “un-edited” protein responsiblefor full-length protein
  • RNA edited protein has premature stop codon creating ApoB-48 (truncated protein)
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28
Q

After chylomicrons enter blood, what happens?

A

the chylomicron receive ApoCII and ApoE from HDL to become a mature chylomicron

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29
Q

HDL function?

A

maintain cholesterol and apoprotein homeostasis

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30
Q

What happens after chylomicron becomes mature?

A

LPL is an extracellular lipase on tissue (muscle/fat) –> ApoCII activates LPL which frees FA to enter tissue for energy or storage
- the remnant chylomicron is recycled in liver and glycerol is recycled in liver as well

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31
Q

What is ApoB-100 good for?

A

it repackages FA and cholesterol taken up by liver from remnant chylomicrons as VLDL –> delivers FA fuels to tissues

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32
Q

Vitamin A

A

biologically active form –> all-trans-retinol

  • can be converted to aldehyde, carboxylic acid, or ester with FA
  • main dietary forms are retinyl-acyl esters and carotenes
  • important for vision! –> deficiency = night blindness, toxicity = blurred vision
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33
Q

Stellate Cells

A

cells in liver that serve as reservoir of Vit A storage

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34
Q

Hepatocytes mediate retinol homeostasis how?

A

retinyl-esters go in (chylomicrons or stellate cells)
retinyl-esters go out (stellate cells or VLDL)
retinol goes out to serum with retinol binding protein

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35
Q

how does retinol help vision?

A
  1. cis-retinal bound to opsin –> rhodopsin
  2. light causes conversion to trans-retinal
  3. activates G-protein
  4. Closure of Na channels
  5. hyperpolarization of rod cell
  6. signal to neuron
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36
Q

Retinoic acid receptors

A

ligand activated transcription factors

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37
Q

Carotenes

A 
uncut = antioxidants
cut = retinal molecules
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38
Q

Vit A deficiency

A

anorexia, retarded growth, increased risk of infection, alopecia, keratinization, night blindness, Bitot’s spots
- dianose by RDR = higher RDR, more body is relying on short-term vitamin A

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39
Q

Vit A toxicity

A

tolerable upper limit is 3000 mg/day

- blurred vision, liver damage

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40
Q

Vitamin E

A

tocopherols –> saturated 16 carbon acyl chains (leafy veggies)
tocotrienols –> polyunsaturated 16 carbon acyl chains (plants oils)
- digestion and absorption parallels fat
- functions in lipid bilayers in intracellular and plasma membranes –> antioxidants
- interactions -> needs Vit C to be regenerated, inhibits Vit K absorption and metabolism

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41
Q

Vit E deficiency

A

RARE unless person has absorption disorder

- myopathy, anemia, neuropathy, ataxia

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42
Q

Vitamin K

A

Carboxylation and Coagulation
phylloquinone –> main form in diet –> leafy veggies
menaquinones –> produced by fermentation
- digestion and absorption parallels fat
- stored in cellular membranes (lung, kidney, marrow, adrenal glands)

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43
Q

Vitamin K as co-factor

A

carboxylates a glutamte residue into zymogen on blood clotting proteins and then Vitamin K epoxide reductase regenerates the co-factor –> this is inhibited by coumadin

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44
Q

Vit K deficiency

A

RARE –> severe deficiency mainfests as coagulation disorder (bleeding)
- no known Vit K toxicity

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45
Q

Vitamin D

A

found in food or animal origin –> most important function is to regulate calcium homeostasis
can be synthesized de novo from cholesterol –> activation requires skin, liver, kidneys

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46
Q

Synthesis of Vitamin D

A

sunlight hits 7-dehydrocholesterol –> hydroxylated twice (once in liver and once in kidney)
- the 1-alpha hydroxylation makes it active (occurs in kidney in response to PTH –> low Ca [ ])

47
Q

Dietary form of Vitamin D

A

cholecalciferol –> absorbed by passive diffusion with fat –> transported to tissue in chylomicrons
25-hydroxycholecalciferol is main form of circulating Vit D and is used to measure status

48
Q

Vitamin D Receptor

A

ligand activated transcription factor –> causes dimerization
- activated VDR increases expression of calcium channel TRPV6, calbindin, and calcium ATPase pumps –> also alters tight junction permeability to calcium

49
Q

Vitamin D deficiency

A

Rickets –> characterized by seizures, growth retardation, failure of bone mineralization
- can be dietary, genetic, or absorptive

50
Q

Vitamin D toxicity

A

most likely vitamin to cause toxicity –> causes calcification of soft tissues

51
Q

Wnt/APC pathway

A

Wnt doesn’t bind –> phosphorylation of beta-catenin by APC complex –> degradation of beta-catenin –> no transcription
Wnt binds –> no phosphorylation of beta-catenin –> activation of APC complex –> activates transcription (cyclin D1 and myc)

52
Q

VDR relation to possible colorectal cancer?

A

people with highest concentration of Vitamin D had reduced incidence of colorectal adenoma
- VDR null mice had elevated cyclin D1 expression and supressed p21 and p27 expression

53
Q

Estimated Average Requirement

A

average daily nutrient intake level estimated to meet requirement of half population
- not a good recommendation

54
Q

Recommended Daily Allowance

A

average daily nutrient intake level sufficient to meet nutritional requirements of 98% of population
- good recommendation

55
Q

Tolerable Upper Limit

A

nutrient intake level that has a risk of overdose

56
Q

Functions of mineral in body

A
  1. Osmotic balance –> MOST Important
  2. Maintaining charge/ [ ] gradients
  3. Enzyme co-factors
  4. Structure –> affects structure of proteins
  5. Taste
57
Q

Major extracellular cation?

A

sodium

58
Q

Major intracellular cation?

A

Potassium

59
Q

Calcium

A

most abundant metal ion in body! –> mostly in bone
Major Functions
1. bone mineralizatoin
2. blood clotting
3. muscle contraction
4. metabolism regulator –> secondary messenger that regulates metabolism in different energy states

60
Q

Calcium absorption

A
  1. Saturable carrier mediate transport
    - TRPvC –> Ca across brush border
    - Calbindin –> chaperones Ca within cell
    - Ca/ATPase –> transports Ca across basolateral side
  2. Pericellular transport –> Claudin (nonsaturable)
61
Q

Things that increase Ca absorption

A

Vitamin D
Sugars/alcohols
Protein

62
Q

Things that decrease Ca absorption

A

Fiber
Phytic/oxalic acids
Divalent cations (Mg and Zn)
unabsorbed fats

63
Q

Calcium sensor??

A

Calmodulin –> can interact with the following

  1. calcineurin –> blocks Ca channels
  2. MLC K –> muscle contraction
  3. Calcium/calmodulin kinase –> inhibits glycogen synthase (work is being done)
  4. Phosphorylase kinase –> activates glycogen phosphorylase
64
Q

Calcium interactions

A
  • Blocks phosphorus uptake –> used to treat hyperphosphatemia
  • Blocks iron uptake
  • Trap fatty acids and bile salts in soaps that are non-digestable (more excretion of bile salts that are normally recycled)
65
Q

Calcium deficiency

A

fat malabsorption disorders

immobilized patients

66
Q

Calcium toxicity

A

Acute –> constipation and bloating
Chronic –> calcification of soft tissue –> CVD
- bone density scan to determine status

67
Q

Magnesium

A
  • Most in bone and soft tissues
    Functions
    1. 70% of bone magnesium associated with phosphorus and calcium in crystal lattice
    2. 30% is amorphous form on surface available for exchange
    3. Intracellularly –> 90% of Mg associated with ATP (essential for kinases and polymerases)
    4. Activation of Vit D requires Mg
68
Q

Magnesium absorption

A
  • TRMP6 –> saturable transport across brush border
  • Basolateral transport –> 2Na/Mg antiporter and K/Na pump
  • Nonsaturable paracellular diffusion
69
Q

Magnesium Interactions

A

Vitamin D
mimic Ca and compete for reabsorption in kidney
inhibits phosphorus absorption by forming precipitate
- Renal excretion before and after loading dose is best

70
Q

Magnesium deficiency

A

dietary not described

Gitelman syndrome –> autosomal recessive mutation in SLC12A3 –> hypomagnesemia, hypokalemia, hypocalcuria

71
Q

Magnesium toxicity

A

epsom salts

- diarrhea, dehydration, flushing, slurred speech, muscle weakness

72
Q

Chloride

A

88% extracellular, 12% intracellular
Functions
1. chloride/bicarb exchanger (enters RBCs in tissues, exits RBCs in lungs)
2. Hypochlorus acid secreted by neutrophils during phagocytosis to neutralize pathogens
3. Gastric HCl by parietal cells

73
Q

Chloride absorption

A

Absorbed paracellularly or through Na/Cl transporter

- only anion secreted by GI cells

74
Q

Potassium

A

Major intracellular cation
Functions
1. generate and maintain electrical potentials –> Na/K ATPase consumes energy to accumulate K in cells
2. Muscle contraction
Regulation
1. Vasopressin and aldosterone increase urinary excretion

75
Q

Potassium absorption

A

Paracellular absorption
K/H ATPase
Basolateral K channel

76
Q

Potassium Interactions

A

decreases Ca excretion

77
Q

Potassium deficiency

A

Hyopkalemia

  • fluid loss, diuretics, refeeding syndrome
  • cardiac arrhythmias, weakness, mental disorientation
78
Q

Potassium toxicity

A

Hyperkalemia

- renal failure and can cause cardiac arrhythmia/arrest

79
Q

Phosphorus

A

85% in bone, 14% in soft tissue, 1% in fluid
Functions
1. Bone mineralization –> calcitonin (bone deposition), calcitriol (bone desorption)
2. Molecules with high energy bonds
3. Acid base balance –> important buffer in kidney

80
Q

Phosphorus absorption

A

Saturable carrier mediated active transport –> when phosphate intake low –> activated by calcitriol
Diffusion –> proximal duodenum (slightly acidic)
INHIBITED BY:
Mg, Aluminum, Calcium (antacids)

81
Q

Regulation of phosphorus

A

Uptake not regulated because its just by diffusion
Excretion promoted by
1. High phosphorus, PTH, acidosis, phosphotonins
Excretion inhibited by
1. low phosphorus, calcitriol, alkalosis, hormones

82
Q

Dents disease

A

X-linked mutation in renal chloride channel –> phosphorus deficiency

83
Q

X-linked hypophosphatemic Rickets

A

mutation in PHEX gene causing elevated FGF-23

84
Q

Autosomal dominant hypophosphatemic Rickets

A

mutation in gene encoding FGF-23 preventing its degradation

85
Q

Iron

A 
either Fe2 (reduced) or Fe3 (oxidized)
Functions
1. Heme synthesis (most important)
2. Iron-sulfur clusters (electron transfer reactions)
3. Non-heme iron
86
Q

Iron Absorption

A

Reductase reduces Fe3 to Fe2 at brush border and then enters cell via DMT1 –> once inside, it’s stored as ferritin –> transport into blood requires oxidation to Fe3 by hephaestin (ceruloplasmin –> copper required) –> Fe3 binds transferritin and transported to tissues

87
Q

Regulation of Iron

A

When iron stores are high, hepcidin is produced as it binds ferroportin and causes degradation

88
Q

Iron Interactions

A

Vit C –> enhances absorption
Copper –> required for export from enterocytes
Zinc –> iron inhibits zinc absorption

89
Q

Iron deficiency

A

anemia, fatigue, listlessness

90
Q

Iron toxicity

A

if it exceeds liver storage capability –> accumulation in tissues –> oxidative dammage
- inherited mutations in hepcidin –> hemochromotosis

91
Q

Copper

A

Functions

  1. co-factor for ceruloplasmin (iron absorption)
  2. Cytochrome C (ETC)
  3. co-factor for lysyl oxidase (collagen synthesis, also requires Vit C)
  4. co-factor for SOD –> antioxidant enzyme
  5. co-factor for dopamine-beta-hydroxylase (catecholamine)
92
Q

Copper absorption

A

Reductase reduces Cu2 to Cu at brush border

  • transported into cell by CTR1
  • enters blood through ATP7A (basolateral transporter)
93
Q

Menkes kinky hair syndrome

A

mutation in ATP7A in gut –> no absorption of copper

- hypothermia, hypotonia, poor feeding, FTT, seizures, hair becomes brittle and sparse

94
Q

Copper deficiency

A

people who eat a lot of zinc or PPI

- anemia, leukopenia, hypopigmentation of skin and hair

95
Q

Copper toxicity

A

acute –> epigastric pain, N/V, diarrhea

chronic –> hematuria, liver and kidney damage

96
Q

Wilson disease

A

mutation in liver specific copper transporter ATP7B –> accumulation of copper in the liver

97
Q

Fiber

A

non-digestable carbohydrates

- reduce absorption of nutrients

98
Q

Cellulose

A

beta-1,4 bonds of glucose –> cannot be digested by humans –> gets digested by microbes

99
Q

Lignins

A

insoluble fiber –> not digestable by bacteria

- branched polymers of phenolic subunits

100
Q

Hemicellulose

A

insoluble fiber –> can be digested by bacteria

101
Q

Pectins

A

soluble fiber

- branched polymer –> almost completely degraded by gut bacteria

102
Q

Gums

A

secreted by plants to close wounds

- completely fermented by gut bacteria

103
Q

beta-glucans

A

soluble fiber –> found in oats and barley

- fermented by gut bacteria to short chain FAs

104
Q

Fructans

A

soluble fiber

- polyfructose –> prebiotics (promote growth of bifidobacteria)

105
Q

Psyllium

A

similar to gums –> quite indigestable but holds a lot of water

106
Q

Resistant starches

A

plant cell walls, starch granules, retrograde starch

- all inaccessible amylose or amylopectin

107
Q

Chitin or chitosan

A

insoluble fibers in exoskeletons of insects/crustaceans

108
Q

What does fiber do?

A

Soluble fiber –> delays gastric emptying, increases transit time and decreases nutrient uptake
Insoluble fiber –> decreases intestinal transit time and increases fecal bulk (decreases nutrient uptake)

109
Q

Glycemic Index

A

measures how much blood glucose increases after digestion

- high fiber foods have lower glycemic index

110
Q

Benefits of fiber?

A
  1. Decreased lipid absorption
  2. Lower serum cholesterol concentrations (increased excretion)
  3. Gut microbiome (prebiotic and generation of short chain FAs)
  4. increases fecal bulk
111
Q

Short Chain Fatty Acids

A
  1. Main energy source for colonic epithelium

2. ligand for GPR43 –> anti-inflammatory, increases IL-10 (makes body tolerant to good gut bacteria)

112
Q

GPR43

A
  1. Anti-inflammatory
  2. expressed on adipocytes –> activation by SCFA inhibits insulin dependent storage of FAs –> increasing their use by other tissues
113
Q

Human breast milk

A

contains human milk oligosaccharides (HMOs)

  • metabolized by gut bacteria –> has immunomodulatory effects
  • act as decoy receptors –> prevent attachment of pathogens to cellular glycolipids and glycoproteins

GI Exam 2 (7 decks)

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