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Nutrition and Metabolism > Exam 3 Material (Cumulative) > Flashcards

Exam 3 Material (Cumulative) Flashcards

1
Q

Cuprous

A

Reduced, Cu1+

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2
Q

Cupric

A

Oxidized, Cu2+

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3
Q

CTR1

A

trasnports Cu1+ (reduced) into enterocyte, trimer

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4
Q

ATP7A

A

copper (Cu1+) exporter, via basolateral membrane of enterocyte to portal blood, ATPase, mutations in this protein cause Menkes’ disease

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5
Q

CCS

A

Copper chaperone for SOD1, delivers copper to SOD1 so copper doesn’t form a new radical

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6
Q

SOD

A

super oxide dismutase

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7
Q

ATOX1

A

delivers copper to TGN (trans golgi network)

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8
Q

Metallothionein (MT)

A

copper storage protein, has 20 cysteines, can bind 7 atoms of copper, zinc storage protein

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9
Q

Factors enhancing copper absorption

A

histidine, methionine, cysteine**, glutathione, citrate

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10
Q

Factors inhibiting copper absorption

A

phytate**, zinc, iron, molydenum, calcium, phosphorus, vitamin C

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11
Q

ATP7B

A

copper exporter in TGN, transports Cu1+ into TGN to be incorporated into ceruloplasmin or to be secreted in bile, mutations lead to Wilson’s disease

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12
Q

Ceruloplasmin (CP)

A

in liver, plasma Cu protein, ferroxidase (oxidizes iron), Cu deficient - decrease Fe release from liver, bad copper assessment (sensitive to acute inflammation)

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13
Q

Hephaestin (HP)

A

ferroxidase (oxidizes iron), copper enzyme in intestine, upregulated in iron deficiency, mutations result in anemia, Cu deficient –> decrease Fe absorption

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14
Q

SOD1

A

antioxidant enzyme, 1 Cu (catalytic) + 1 Zn (structural), catalyzes dismutation of superoxide -> converts it to hydrogen peroxide, in mitochondria for ETS

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15
Q

Dopamine monooxygenase

A

dopamine beta-hydroxylase, converts dopamine to norepinephrine, vitamin C reduces Cu2+ to Cu1+ so it can work on dopamine

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16
Q

Lysyl oxidase

A

Cu-containing extracellular enzyme that crosslinks collagens or elastin to extracellular matrix, deaminates lysine in presence of O2

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17
Q

Tyrosinase

A

Cu-containing enzyme that converts tyrosine to melanin for skin darkening, copper deficiency can cause albinism

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18
Q

Neutropenia

A

low leukocytes

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19
Q

Menkes disease

A

mutation of ATP7A gene, x-linked recessive, rare, transport of Cu out of intestine is impaired, kinky hair disease (slow growth, hypothermia, seizures, degeneration of brain tissue, defective arterial walls, depigmentation of skin and hair, death at young age), treated with daily cu-histidine injections

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20
Q

Wilson’s disease

A

copper overload, rare, autosomal recessive mutation of ATP7B, too much Cu in liver leaks into blood to other organs, can be fatal, unbound Cu, hemolytic anemia, organ damage, liver/brain/kidneys, cornea of eye, treated with penicillamine or zinc

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21
Q

Penicillamine

A

chelation therapy, binds copper for excretion, treatment for Wilson’s disease

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22
Q

Kayser-Fleisher ring

A

cornea of eye has copper build up so copper atoms form rings around eye

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23
Q

Ferrous

A

Fe2+, bioavailable because it will be soluble in intestine, reduced, precipitates out at high pH

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24
Q

Ferric

A

Fe3+, oxidized, precipitates out at low pH, less bioavailable

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25
DMT1
DMT1 transports Fe2+ through apical membrane with Dcytb, mutations cause anemia, induced by iron deficiency, needed for erythropoiesis
26
Dcytb
ferrireductase (duodenal cytochrome b), reduces Fe3+ to Fe2+ for absorption into enterocyte via DMT1, induced by iron deficiency, utilizes ascorbate
27
Ferroportin
export iron at basolateral membrane of enterocyte, induced by iron deficiency (or iron loading at macrophage), main regulated point of entry for iron
28
Hephaestin
ferroxidase, oxidize Fe2+ to Fe3+ so it can bind transferrin, basolateral surface of enterocyte, induced by iron deficiency, mutation results in anemia
29
Transferrin
transports iron to RBC for erythropoiesis, has IRE at 3'UTR, receptor upregulated by iron deficiency, receptor downregulated in adequate iron
30
Erythroid aminolevulinic acid synthase
rate limiting enzyme in heme biosynthetic pathway, needs iron
31
RES
reticuloendothelial system, macrophages of liver/spleen/bone marrow, ingest old RBCs to recycle iron, large storage reservior for iron
32
Ferritin
iron storage protein, all cells, mRNA has IRE at 5'UTR, downregulated when low iron (so iron to store), upregulated when adequate iron, good indicator of status for iron overload, also inflammation/infection/chronic disease
33
Hepcidin
iron-regulatory hormone, produced in liver, secreted into circulation, induced by iron, production shuts off in iron deficiency, breaks of iron absorption, binds ferroportin in adequate iron status to block absorption
34
ZIP14
hepatocyte takes up non-transferrin-bound-iron in iron overload conditions, also zinc
35
Hemoglobin
functional iron indicator, common for iron deficiency, poor indicator, RBC 120 days, low Hb can be due to other things
36
Transferrin saturation
% sat TIBC = serum Fe/TIBC * 100
37
ZIP4
transport protein for Zn2+ across apical membrane of enterocyte (saturable)
38
ZNT1
transport protein for Zn2+ across basolateral membrane of enterocyte (saturable)
39
Acrodermatitis enteropathica
zinc malabsorption from genetic mutation of ZIP4, dermatitis, impaired immunity, impaired wound healing, hair loss, anorexia, impaired taste acuity
40
Carbonic Anhydrase
zinc metalloenzyme, interconverts CO2 and bicarb to maintain acid-base balance in blood (buffer), coordinated by histidine
41
Carboxypeptidase A
digestive enzyme in pancreas, hydrolyzes peptide bonds, histidine and glutamic acid coordinate
42
Zinc finger protein
most common DNA binding domain, C4 nuclear receptores (4 cysteines - RAR & VDR), C2H2 (2 cysteines, 2 histidines) depends where zinc coordinated, activate or inhibits expression of target genes
43
Ananda Prasad
expert on zinc, helped patient with anemia, hypogonadism, and dwarfism (21 yo looks like 8 yo) by supplementing with zinc
44
Prevalence of zinc deficiency
Countries that don't consume a lot of meat/fish like India, Nepal, sub-saharan Africa
45
Glutathione Peroxidase 1
first selenoprotein, >50% total body Se, antioxidant enzyme, Se buffer
46
Selenoprotein P
main Se plasma transport protein, transports ~90% plasma Se, up to 10 molecules Se at a time
47
Iodothyronine Deiodinase
selenoenzymes (3), converts T4 (thyroxine) to T3 (active form), Se deficiency decreases activity, but compensation
48
Thioredoxin Reductase
selenoenzyme that reduces thioredoxin (an antioxidant), aka regenerates it, main function of Se
49
Selenoprotein W (SELW)
small Se protein in muscle, causes white muscle disease, prevent with soil supplementation of Se
50
Keshan disease
causes cardiomyopathy from selenium deficiency in Keshan province of China, eradicated due to Se supplementation
51
Kashin-Beck disease
Northern China and Russia (low Se soil), disease of cartilage, Se supplementation does not cure it, iodine deficiency or toxin contamination may be why
52
Myxedematous Cretinism
Se deficiency, thyroid enlargement and decreased intelligence, Se and Iodine contribute, Se supplement alone makes it worse
53
Selenosis
change in nail structure, loss of nails, and hair, lesions of skin/nervous system, nausea, weakness, diarrhea, Se intake of 3.2-6.7 mg/day, no antidote
54
Acute Se Toxicity
gram quantities of Se, GI and neurological disturbances, Myocardial infarction, renal failure, acute respiratory distress syndrome, no antidote
55
Methylselenol
Major urinary form of selenium
56
Iodate
used in fortification of grains, high bioavailability
57
Thyroid Hormone function
postnatal growth in stature, bone maturation, BMR, regulator of prenatal cell growth (neuronal, peripheral tissues)
58
Thyroid hormone mechanism
TSH from pituitary gland stimulates thyroid gland to produce thyroid hormone, hormone taken up, enters nucleus, binds to THR, affects translation of proteins
59
Goiter
tracheal/esophagus pressure, damage to laryngeal nerves, respiratory difficulty, hoarseness
60
Cretinism (late pregnancy)
shorter stature, mental retardation, hypothyroidism
61
Cretinism (early pregnancy)
neurologic, inner ear/brain defect, short stature fur normal, spasticity of legs, deaf mutism, goiter
62
Hyperatremia because
diuretics, disease with rental tube damage, chronic V/D, Addison's disease, exercise-induced, hypovolemia, lethargy, confusion, weakness
63
Carbohydrates
primary metabolic fuel, 40-60% energy, primarily consumed as glucose (polymers) and simple sugars, disturbances of glucose metabolism is common disorder
64
SGLT1
Sodium Glucose Transporter 1, 1:1:260 glucose:sodium:water into enterocyte from apical membrane
65
Vitamins necessary for CHO metabolism
thiamin (b1), riboflavin (b2), niacin (b3), pyridoxine (b6), biotin
66
Endogenous proteins
desquamated mucosal cells, digestive enzymes and glycoproteins
67
Elderly Protein Requirement
1 g/kg instead of 0.8 g/kg
68
Endurance Exercise Protein Requirement
1.4 g/kg, increased AA oxidation because you are using protein for fuel
69
Protein better for resistance exercise
whey and casein, not soy
70
Heavy Resistance Exercise Protein Requirement
1.8 g/kg recommended, up to 2.4 g/kg does not increase whole body protein synthesis but AA oxidation increases
71
Trypsin
enteropeptidase secreted from duodenum converts trypsinogen to trypsin, trypsin converts procarboxypeptidase to carboxypeptidase, and chymotrypsinogen to chymotrypsin
72
Essential AA
TV TILL PM: tryptophan, valine, threonine, isoleucine, leucine, lysine, phenylalanine, methionine, and sometimes histidine
73
Methionine can be converted to
cysteine
74
Phenylalanine can be converted to
tyrosine

Nutrition and Metabolism (3 decks)

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