Bhl Week 1: Iron Metabolism

Front 1

Iron is most abundant in which form?

Is this form soluble?

Back 1

Fe3+ (ferric) form

*Relatively insoluble; must be converted to Fe2+ or become part of a heme molecule to be absorbed in GI tract

Front 2

How does the body primarily regulate iron stores?

Back 2

By adjusting iron absorption from the GI tract

Front 3

What is the amount of obligate iron loss per day for adult men and non-menstruating women and for menstruating women?

Back 3

Adult men/non-menstruating women = 1 mg/day

Menstruating women = 2 mg/day

Front 4

List 2 mechanisms by which iron absorption is controlled.

Which form of regulation is stronger?

Back 4

1. Iron stores (absorption inversely proportional to body iron stores)
2. Erythropoiesis (increases iron absorption)

*Erythropoiesis can override "stores regulator"

Front 5

Name the iron transport molecule in blood.

Back 5

Transferrin

Front 6

Name the primary iron storage molecule.

Back 6

Ferritin

Front 7

Name the primary iron regulatory molecule

Back 7

Hepcidin

Front 8

What does the transferrin receptor have the highest avidity for?

Back 8

Transferrin containing 2 iron atoms

Front 9

If a person is not sick, how does the ferritin level in the blood relate to body iron stores?

What happens to the ferritin level in states of inflammation?

Back 9

Directly proportional

*Ferritin level increases in states of inflammation; So, if a person is sick, the ferritin level can't be used to estimate body iron stores

Front 10

What is the effect of hepcidin on iron absorption from the GI tract?

Back 10

Decreases iron absorption from GI

(Also blocks iron release from macrophages).

Front 11

What is the result of hepcidin overexpression?

Back 11

Anemia

Front 12

Iron absorption primarily occurs in which portion of the GI tract?

Back 12

Duodenum

Front 13

Iron in the diet comes from which 2 forms?

How are these absorbed?

Back 13

1. Heme iron --> readily absorbed into enterocyte
2. Non-heme --> Fe3+; must be converted to Fe2+ to be absorbed

Front 14

Iron absorption can only be increased to a limited extent. What is the maximum about of Fe that can be absorbed from the GI tract per day?

Back 14

4 mg per day

Front 15

Which form of iron is absorbed directly and relatively easily into the enterocyte?

Back 15

Heme ring with Fe attached

Front 16

Once inside the enterocyte, what are the 2 fates of iron?

Back 16

1. Transferred to the plasma at the basolateral side of the enterocyte
2. Stored in the enterocyte in the form of ferritin

Front 17

Which transport protein mediates the release of iron from the enterocyte into the plasma?

Back 17

Ferroportin
(universal iron export mechanism)

Front 18

How does hepcidin inhibit Fe export from enterocytes?

Back 18

Hepcidin blocks ferroportin

Front 19

What must happen to iron before it can be bound to transferrin in the plasma?

Back 19

Ferrous form (Fe2+) must be converted to ferric form (Fe3+)

Front 20

How does gastric acid assist iron absorption?

Back 20

It is required for the conversion of ferric form (Fe3+) to ferrous form (Fe2+).

Front 21

List 2 dietary factors that increase Fe absorption.

Back 21

1. Ascorbic acid
2. Human breast milk

Front 22

List 6 factors that decrease Fe absorption.

Back 22

1. Decreased gastric acid
2. Phytates in grains
3. Tannates in tea
4. Phosphates
5. Some vegetable proteins
6. Cow's milk proteins

Front 23

How is the synthesis of key molecules (transferrin, ferritin, etc.) regulated?

Back 23

By intracellular iron level

Front 24

What are IRPs and IREs?

Back 24

Iron regulatory proteins (IRPs)
Iron responsive elements (IREs)

Front 25

An IRP under iron-depleted conditions will bind to which end of mRNA? (5' or 3')

Back 25

5' (Iron allows translation)

Front 26

Iron blocks translation of iron-related molecule genes on which end of the mRNA?

Back 26

3' (iron blocks translation)

Front 27

Most of the iron being transported by transferrin in your blood is derived from where?

Back 27

Normal breakdown of senescent RBCs by macrophages of the RES

Front 28

Where is hepcidin synthesized and what factors stimulate its production?

Back 28

Liver

*Synthesized in response to inflammatory cytokines and iron excess

Front 29

What is the affect of hepcidin on macrophages?

Back 29

Blocks release of iron from macrophaghes

Front 30

What conditions result in decreased hepcidin synthesis?

Back 30

1. Iron deficiency
2. Hypoxia
3. Increased erythropoietin

Front 31

What molecule is produced by the HAMP gene in the liver?

Back 31

Hepcidin

Front 32

List 4 markers of iron status.

Back 32

1. Serum iron level
2. Transferrin level (Total Iron Binding Capacity; TIBC)
3. Transferrin saturation
4. Serum ferritin

Front 33

Do transferrin levels increase or decrease in iron deficiency?

What about in inflammation?

Back 33

INCREASE in iron deficiency

DECREASE in inflammation

Front 34

Do ferritin levels increase or decrease in iron deficiency?

What about in inflammation?

Back 34

DECREASE in iron deficiency

INCREASE in inflammation (acute phase reactant)