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MCC > Wk 1 TBL 2 Nutrition: Iron, Mineral Metabolism > Flashcards

Wk 1 TBL 2 Nutrition: Iron, Mineral Metabolism Flashcards

1
Q

List essential micronutrients

A

Macrominerals:
1. calcium
2. chlorine
3. magnesium
4. phosphorus
5. potassium
6. sodium
7. sulfur

Trace minerals:
1. copper
2. iodine
3. iron
4. manganese
5. molybdenum
6. selenium
7. zinc
8. fluoride

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2
Q

List essential macronutrients for humans

A

Fat
PRO
CHO

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3
Q

Describe the life-cycle of iron homeostasis

A

managed more at the level of protein synthesis (translation of mRNA to PRO) than at the level of transcription (mRNA synthesis).

Regulation of the synthesis of the transferrin receptor-1 (TfR-1) and divalent metal transporter-1 (DMT-1), responsible for the uptake of iron by cells
regulation of the iron uptake proteins and the iron storage protein occurs through posttranscriptional modification of TfR-1 and ferritin messenger RNAs (mRNAs)

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4
Q

What is the role of transferrin?

A

Carry iron around in the body
-carries 2 ferric (Fe3+)

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5
Q

What is the role of ferritin?

A

Store iron (primarily in the liver)

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6
Q

What is the role of ferroportin and DMT1?

A

-Transport iron across enterocyte membranes

-DMT1 is also responsible for the transport of zinc, copper and cobalt

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7
Q

What is the role of hepcidin?

A

Decreases plasma [iron] by:
1. blocking ferroportin in enterocytes
2. blocking ferroportin in the liver

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8
Q

What is the role of HFE?

A

Regulate the production of hepcidin

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9
Q

What is the role of transferrin receptor?

A

Bind Fe2+ to the apical surface of enterocytes to allow iron absorption

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10
Q

How does altered iron homeostasis (anemia & iron overload) affect different organs and tissues?

A

Anemia:
1. mitochondria fxn inhibited b/c iron is a cofactor
2. arrhythmias -> enlargement
3. confusion, depression
4. low O2 -> can affect all organ systems
Overload:
1. Liver disease, cirrhosis
2. Heart dysfunction, failure
3. hypothyroid
4. pancreatic islet cell damage -> diabetes
5. hypogonadism
6. immune system dysfunction
7. renal dysfunction

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11
Q

Compare iron deficiency anemia with anemia of chronic disease and hemochromatosis

A
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12
Q

What are signs of iron deficiency?

A

Fatigue
pale conjunctiva and skin
weakness
cold extremities
arrhythmias, palpitations
SOB
Kids - behavioral, frequent infections

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13
Q

What are signs of copper deficiency?

A

anemia
leukopenia
chronic: neurologic and growth defects in children

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14
Q

What are signs of zinc deficiency?

A

Growth retardation
hair loss
skin lesions (acrodermatitis)
diarrhea
delayed wound healing

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15
Q

How is dietary iron absorbed?

A

Iron:
1. heme (fe2+) picked up by heme transporter on enterocytes
2. non-heme iron (fe3+) is first reduced to Fe2+ then taken in by DMT1 (divalent metal transporter)
3. some binds ferritin while other transported over via ferroportin 1
4. Fe2+ oxidized to Fe3+ and picked up by transferrin
5. Goes to either erythroid marrow or to liver
6. Hepcidin produced by liver -> downregulation of ferroportin 1 protein

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16
Q

What are the primary uses for iron?

A

Hb production
Transport O2 in Hb and myoglobin
DNA synthesis
Respiration and energy metabolism
Synthesis of collagen and some NTs
Immune fxn

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17
Q

What are the primary uses for copper?

A

Needs for many enzymes:
1. ceruloplasmin, a blood protein req’d for oxidizing Fe2+ to Fe3+, which allows it to bind to transferrin
2. monoamine oxidase
3. cytochrome C oxidase (complex IV of the respiratory chain)
4. superoxide dismutase
5. hephaestin (HEPH), a copper-dependent ferroxidase needed for iron transport from enterocytes to blood

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18
Q

What are the primary uses for zinc?

A
  1. Req’d cofactor of many enzymes like alkaline phosphatase, superoxide dismutase
  2. Req’d in structural proteins like Zn-finger transcription factor
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19
Q

What is the role of hepatocytes in iron homeostasis?

A

Produce hepcidin, which downregulates ferroportin 1, the protein that takes iron from the enterocytes into blood

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20
Q

What is the role of enterocytes in iron homeostasis?

A

Absorb Fe2+ from the lumen of sm intestine

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21
Q

What is the role of macrophages in iron homeostasis?

A

Digest RBCs and recycle iron

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22
Q

Can one be iron deficient with a normal Hb and Hct?

A

Yes, anemia is a later symptom of iron deficiency

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23
Q

Dietary sources of iron

A

red meats, fish, poultry, fortified cereals, spinach, beans, tomatoes, etc

24
Q

How can iron absorption be increased?

A
  1. iron in diet as heme (Fe2+) (high bioavailability)
  2. vit C consumed w/ non-heme iron
25
Q

What decreases iron absorption?

A
  1. chelators - binds to iron in Fe3+ state in GI, prevents it from being reduced to Fe2+ so it cannot be absorbed
  2. calcium - prevents binding of chelators so Fe3+ can be reduced and taken up by cells
26
Q

What are some natural chelators?

A

oxalates - found in spinach
polyphenols - veggies

27
Q

What can cause iron deficiency in infants?

A
  1. iron deficiency during pregnancy -> infant iron deficiency b/c they are very dependent on their fetal stores
  2. breast milk has low [iron] but it’s very bioavailable
  3. feeding an infant (<12 mos) cow’s milk -> iron deficiency b/c it causes increased sloughing of enterocytes
28
Q

What are downsides to iron fortified foods?

A

Iron overload:
1. 1/100-200 Americans have hemochromatosis -> beta-cell destruction
2. high serum ferritin and dietary (heme) iron associated w/ diabetes

Iron poisoning:
1. corrosive to GI mucosa-> unregulated absorption
2. systemic affects on heart, lungs, and liver incl acidosis

29
Q

What is used to tx iron poisoning?

A

deferoxamine, an iron chelator

30
Q

How are zinc and copper absorbed?

A
31
Q

What foods are abundant in zinc?

A

seafood
meats
beans
dairy
nuts

32
Q

When are copper deficiencies seen?

A

Rare but can be seen when
1. zinc supplements are taken in excess
2. Menkes disease - X-linked mutation in a copper transporter

33
Q

What is the daily iron requirement?

A

10-20 mg
heme (ferrous) iron = Fe2+
ferric iron = Fe2+

34
Q

What form of iron is absorbed by enterocytes?

A

Fe2+
so, Fe3+ must be converted

35
Q

What enzyme converts Fe3+ to Fe2+?

A

Vitamin C ferrireductase on the apical size of enterocytes

36
Q

What is the iron cotransporter across the enterocyte apical membrane?

A

Divalent metal transporter 1 (DMT1) - through which Fe2+ crosses the membrane, H+ is also taken in

37
Q

What happens to iron after it’s absorbed into the enterocyte?

A
  1. Can be oxidized back to Fe3+ and stored as ferritin
  2. Fe2+ can be transported around the body - mostly carried to liver and BM
38
Q

How does iron leave enterocytes?

A

Through a transporter on the basal surface called ferroportin (Ireg-1) as Fe2+

39
Q

What happens to iron after it’s in circulation?

A

Hephaestin converts Fe2+ (ferrous) to Fe3+ (ferric) form

40
Q

What is apotransferrin?

A

Unbound transferrin the blood

41
Q

What are the 2 primary fates for iron?

A
  1. ~75% to the BM for erythropoiesis. Iron used for Hb to carry O2
  2. ~10-20% transferrin carries iron to liver where it is stored in ferric form (Fe3+) as ferritin
42
Q

How does iron enter the liver?

A

There is a transferrin receptor on the hepatocyte membrane that endocytoses the transferrin w/ iron attached.

43
Q

What happens after transferrin enters the hepatocyte?

A
  1. A vesicle forms around the transferrin
  2. H+ enters the vesicle -> decreased pH, which causes expression of DMT on the vesicle membrane and detachment of the transferrin/Fe3+
  3. Fe3+ (ferric) reduced to Fe2+ (ferrous), released into cytosol w/ H+
  4. Fe2+ oxidized to Fe3+ (ferric) so it can be stored as ferritin w/in hepatocyte
  5. vesicle releases transferrin back into circulation
44
Q

What factors regulate plasma [iron]?

A
  1. hepcidin - produced and secreted by liver
    -inhibits fxn of ferroportin (transporter on basal surface of enterocytes), so prevents release of iron into circulation, decreasing plasma [iron]
    -blocks ferroportin in spleen to block splenic macrophages that breakdown RBCs from releasing iron into circulation
45
Q

What stimulates hepcidin release?

A
  1. cytokines like IL-6
  2. increased [iron] (attached to transferrin)
  3. LPS (pathogenic components)
  4. HFE protein made by HFE gene (AKA hemochromatosis gene) is the primary regulator as it regulates the production of hepcidin
46
Q

What happens if there is a mutation of the HFE gene?

A

Hereditary hemochromatosis

47
Q

What happens with hemochromatosis?

A

Iron overload b/c hepcidin is not acting to block absorption in the intestines, from the liver, or from splenic macrophages

48
Q

What is hemosiderosis?

A

Iron deposition in tissue

49
Q

What is hemochromatosis?

A

Excess iron that -> organ damage due to free radical formation which damage the cell through lipid peroxidation, fibrosis & collagen deposition, and DNA damage

50
Q

What is primary hemochromatosis?

A

Hereditary - autosomal recessive
-most common mutation in HFE gene (C282Y) but could also be due to mutations in the transferrin receptor (TFR2), or the hepcidin gene - HAMP
-> excess absorption of Fe2+

51
Q

What is secondary hemochromatosis?

A

Due to transfusions (as w/ beta-thalassemia), excessive iron intake, chronic liver disease, porphyria cuteana tarda

52
Q

What 3 genes control hepcidin production?

A
  1. TFR-2
  2. HJV: hemojuvelin
  3. HFE- encodes hepcidin
53
Q

How does hemochromatosis present?

A

males 40 yo/ females 50yo
Common triad:
1. cirrhosis -> hepatocellular carcinoma
2. DM2
3. bronze skin

Other symptoms:
-dilated cardiomyopathy
-hypogonadism
-arthropathy (CPPD (arthritis) calcium pyrophosphate - Ca2+ in joints)

54
Q

What is tx for hemochromatosis?

A
  1. phlebotomy
  2. deferiprone (chelation therapy) feri = ferric
55
Q

What do labs look like w/ hemochromatosis?

A

increased ferritin, iron, % saturation ferrition
decreased TIBC
definitive w/ transferrin > 45 and serum ferritin >200 m, >150 females

56
Q

Compare Wilson’s w/ hemochromatosis

A

Wilson’s: excess copper
age: teens-20’s (<40 yo)
mechanism: decreased excretion of copper

Hemochromatosis: excess iron
age: 40+, 50+
mechanism: increased absorption of iron

MCC (44 decks)

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