Nutrition Flashcards

(113 cards)

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
What happens to the FAs once absorbed?
FAs are re-esterified to glycerol to make TAG in epithelial cells
26
ApoB-48
major apoprotein of chylomicrons from dietary fats | - encoded by same gene that makes ApoB-100
27
ApoB-100
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)
28
After chylomicrons enter blood, what happens?
the chylomicron receive ApoCII and ApoE from HDL to become a mature chylomicron
29
HDL function?
maintain cholesterol and apoprotein homeostasis
30
What happens after chylomicron becomes mature?
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
31
What is ApoB-100 good for?
it repackages FA and cholesterol taken up by liver from remnant chylomicrons as VLDL --> delivers FA fuels to tissues
32
Vitamin 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
33
Stellate Cells
cells in liver that serve as reservoir of Vit A storage
34
Hepatocytes mediate retinol homeostasis how?
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
35
how does retinol help vision?
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
36
Retinoic acid receptors
ligand activated transcription factors
37
Carotenes
``` uncut = antioxidants cut = retinal molecules ```
38
Vit A deficiency
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
39
Vit A toxicity
tolerable upper limit is 3000 mg/day | - blurred vision, liver damage
40
Vitamin E
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
41
Vit E deficiency
RARE unless person has absorption disorder | - myopathy, anemia, neuropathy, ataxia
42
Vitamin K
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)
43
Vitamin K as co-factor
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
44
Vit K deficiency
RARE --> severe deficiency mainfests as coagulation disorder (bleeding) - no known Vit K toxicity
45
Vitamin D
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
46
Synthesis of Vitamin D
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
Dietary form of Vitamin D
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
Vitamin D Receptor
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
Vitamin D deficiency
Rickets --> characterized by seizures, growth retardation, failure of bone mineralization - can be dietary, genetic, or absorptive
50
Vitamin D toxicity
most likely vitamin to cause toxicity --> causes calcification of soft tissues
51
Wnt/APC pathway
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
VDR relation to possible colorectal cancer?
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
Estimated Average Requirement
average daily nutrient intake level estimated to meet requirement of half population - not a good recommendation
54
Recommended Daily Allowance
average daily nutrient intake level sufficient to meet nutritional requirements of 98% of population - good recommendation
55
Tolerable Upper Limit
nutrient intake level that has a risk of overdose
56
Functions of mineral in body
1. Osmotic balance --> MOST Important 2. Maintaining charge/ [ ] gradients 3. Enzyme co-factors 4. Structure --> affects structure of proteins 5. Taste
57
Major extracellular cation?
sodium
58
Major intracellular cation?
Potassium
59
Calcium
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
Calcium absorption
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
Things that increase Ca absorption
Vitamin D Sugars/alcohols Protein
62
Things that decrease Ca absorption
Fiber Phytic/oxalic acids Divalent cations (Mg and Zn) unabsorbed fats
63
Calcium sensor??
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
Calcium interactions
- 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
Calcium deficiency
fat malabsorption disorders | immobilized patients
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Calcium toxicity
Acute --> constipation and bloating Chronic --> calcification of soft tissue --> CVD - bone density scan to determine status
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Magnesium
- 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
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Magnesium absorption
- TRMP6 --> saturable transport across brush border - Basolateral transport --> 2Na/Mg antiporter and K/Na pump - Nonsaturable paracellular diffusion
69
Magnesium Interactions
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
Magnesium deficiency
dietary not described | Gitelman syndrome --> autosomal recessive mutation in SLC12A3 --> hypomagnesemia, hypokalemia, hypocalcuria
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Magnesium toxicity
epsom salts | - diarrhea, dehydration, flushing, slurred speech, muscle weakness
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Chloride
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
Chloride absorption
Absorbed paracellularly or through Na/Cl transporter | - only anion secreted by GI cells
74
Potassium
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
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Potassium absorption
Paracellular absorption K/H ATPase Basolateral K channel
76
Potassium Interactions
decreases Ca excretion
77
Potassium deficiency
Hyopkalemia - fluid loss, diuretics, refeeding syndrome - cardiac arrhythmias, weakness, mental disorientation
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Potassium toxicity
Hyperkalemia | - renal failure and can cause cardiac arrhythmia/arrest
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Phosphorus
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
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Phosphorus absorption
Saturable carrier mediated active transport --> when phosphate intake low --> activated by calcitriol Diffusion --> proximal duodenum (slightly acidic) INHIBITED BY: Mg, Aluminum, Calcium (antacids)
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Regulation of phosphorus
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
Dents disease
X-linked mutation in renal chloride channel --> phosphorus deficiency
83
X-linked hypophosphatemic Rickets
mutation in PHEX gene causing elevated FGF-23
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Autosomal dominant hypophosphatemic Rickets
mutation in gene encoding FGF-23 preventing its degradation
85
Iron
``` either Fe2 (reduced) or Fe3 (oxidized) Functions 1. Heme synthesis (most important) 2. Iron-sulfur clusters (electron transfer reactions) 3. Non-heme iron ```
86
Iron Absorption
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
Regulation of Iron
When iron stores are high, hepcidin is produced as it binds ferroportin and causes degradation
88
Iron Interactions
Vit C --> enhances absorption Copper --> required for export from enterocytes Zinc --> iron inhibits zinc absorption
89
Iron deficiency
anemia, fatigue, listlessness
90
Iron toxicity
if it exceeds liver storage capability --> accumulation in tissues --> oxidative dammage - inherited mutations in hepcidin --> hemochromotosis
91
Copper
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
Copper absorption
Reductase reduces Cu2 to Cu at brush border - transported into cell by CTR1 - enters blood through ATP7A (basolateral transporter)
93
Menkes kinky hair syndrome
mutation in ATP7A in gut --> no absorption of copper | - hypothermia, hypotonia, poor feeding, FTT, seizures, hair becomes brittle and sparse
94
Copper deficiency
people who eat a lot of zinc or PPI | - anemia, leukopenia, hypopigmentation of skin and hair
95
Copper toxicity
acute --> epigastric pain, N/V, diarrhea | chronic --> hematuria, liver and kidney damage
96
Wilson disease
mutation in liver specific copper transporter ATP7B --> accumulation of copper in the liver
97
Fiber
non-digestable carbohydrates | - reduce absorption of nutrients
98
Cellulose
beta-1,4 bonds of glucose --> cannot be digested by humans --> gets digested by microbes
99
Lignins
insoluble fiber --> not digestable by bacteria | - branched polymers of phenolic subunits
100
Hemicellulose
insoluble fiber --> can be digested by bacteria
101
Pectins
soluble fiber | - branched polymer --> almost completely degraded by gut bacteria
102
Gums
secreted by plants to close wounds | - completely fermented by gut bacteria
103
beta-glucans
soluble fiber --> found in oats and barley | - fermented by gut bacteria to short chain FAs
104
Fructans
soluble fiber | - polyfructose --> prebiotics (promote growth of bifidobacteria)
105
Psyllium
similar to gums --> quite indigestable but holds a lot of water
106
Resistant starches
plant cell walls, starch granules, retrograde starch | - all inaccessible amylose or amylopectin
107
Chitin or chitosan
insoluble fibers in exoskeletons of insects/crustaceans
108
What does fiber do?
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
Glycemic Index
measures how much blood glucose increases after digestion | - high fiber foods have lower glycemic index
110
Benefits of fiber?
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
Short Chain Fatty Acids
1. Main energy source for colonic epithelium | 2. ligand for GPR43 --> anti-inflammatory, increases IL-10 (makes body tolerant to good gut bacteria)
112
GPR43
1. Anti-inflammatory 2. expressed on adipocytes --> activation by SCFA inhibits insulin dependent storage of FAs --> increasing their use by other tissues
113
Human breast milk
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