Minerals Flashcards
transferrin
transports iron in the blood between the intestine, RES, and bone marrow
ferritin and hemosiderin
storage forms of iron, found in the liver and RES
two forms of injested iron
heme and non-heme
which form of iron is more bioavailiable?
heme iron
How is heme iron absorbed?
remains bound to heme, transported by Heme carrier protein 1 in the duodenum and jejunum, binds to ferritin in the enterocyte
How is non-heme iron absorbed?
it is first reduced to the 2+ form by Dcytb and then transported to the enterocyte by DMT1
duodenal cytochrome B
reduces heme from 3+ to 2+ in the intestines
DMT1
transports Fe2+ into the enterocyte
ferric hydroxide
complexes with iron to prevents its absorption
factors that enhance non-heme absorption
acids (help solubilize), chelation by organic molecules, upregulation of DMT1 because of deficiency
factors that impair iron absorption
polyphenols, oxalic acid, phytates, phosphorylated serine, calcium, phosphate, zinc, magnesium, nickel
ferroportin 1
transports iron out of the enterocyte and into the blood
hephaestin
oxidized iron to Fe3+ form
how does iron get exported to the circulation
It leaves the cell through ferroportin and then gets oxidized to Fe3+ by hephaestin, and finally it binds to transferrin
transferrin receptor
binds circulating transferrin and iron is taken up into the cell
most common deficinecy worldwide is
iron
hepcidin
regulates iron efflux into circulation from intestine, liver, spleen and lymph nodes
how is iron absorption regulated by hepcidin
when hepcidin levels increase, iron is stored in the body and when levels decrease, iron is released. This occurs due to the expression of ferroportin on the basolateral membranes of enterocytes
glossitis and angular stomatitis
red tongue and lips from an iron deficiency
koilonychia
bending of the nails from iron deficiency
hereditary hemochromatosis
defect in hepcidin, results in too much iron in the blood, treated by bleeding
risk factors of copper deficiency
upper gastrointestinal surgery, zinc supplements, malabsorption, Menke’s Celiac
Manifestations of copper deficiency
neurologic (peripheral neuropathy), hematologic, iron deficiency
Wilson’s disease
copper overload due to mutations in the copper ATPase leading to copper accumulation in the liver
Menke’s disease
mutation in copper transporter, results in copper deficiency
metallothionein
binds both copper and zinc in the enterocyte but has a higher affinity for copper, when there is too much zinc in the diet, MT is overexpressed resulting in a copper deficiency
vitamin C and iron
VC helps keep iron in its reduced form and increases absorption
transporters of copper
DMT1 and Crt
copper deficiency is similar to a deficiency in
vitamin B12
transporters of zinc
DMT1 and ZIP4
