ions, vitamins and minerals lecture Flashcards
sequential molar concentrations (factor 10^-3)
molar, millimolar, micromolar, nanomolar, picomolar, femtomolar
define diffusion
process where atoms or molecules intermingle due to random thermal motion; fast over microscopic distances, slow over macroscopic differences
purpose of circulatory system in multicellular organisms
bring individual cells within diffusion range
function of cell membrane
act as diffusion barrier so cells can have different cytoplasmic concentrations vs. EC
water potential from low to high
hypotonic (swell), isotonic, hypertonic (shrink)
how do molecules cross epithelium to enter bloodstream
paracellular transport through tight junctions and lateral intercellular spaces; transcellular transport
through epithelial cells in apical membrane
2 types of transport proteins involved in faciliated diffusion or active transport
channel proteins (form aqueous pores - fast), carrier proteins (bind to solute and undergo conformational change - slow)
4 types of gated channel-mediated transport
voltage-gated, EC ligand-gated, IC ligand-gated, mechanically gated
3 types of carrier-mediated transport
uniport, symport (same direction), antiport (opposite direction - equalise charge); secondary active transport
define primary active transport
linked directly to cellular metabolism, using ATP to power transport
define secondary active transport
derives energy from concentration gradient of another substance that is actively transported
effect of facilitated diffusion on rate of substance flowing down concentration gradient
enhances, but tends to equilibrate substance across membrane
how is absorption of glucose and galactose achieved
secondary active transport, with SGLT-1 carrier protein on apical membrane, which can transport glucose against concentration gradient
how is absoprtion of fructose achieved
facilitated diffusion using GLUT-5 carrier protein on apical membrane, which is effective at low concentrations of fructose in lumen as tissue and plasma levels low
how does glucose exit basolateral membrane
facilitated diffusion through GLUT-2 carrier protein (high-capacity, low-affinity); glucose between plasma and enterocyte generally equilibrated as glucose moves out to blood
what requires specific absorption
water and ions, calcium, iron, vitamins (B12)
where is most water absorbed
jejunum in small intestine (small intestine: 8L, colon: 1.4L)
how are most ions slowly absorbed
passive diffusion
source of water
ingest, saliva, gastric secretions, bile, pancreas, intestinal
what drives standing gradient osmosis
Na+ (transported from lumen into enterocyte, which becomes more efficient down intestine)
Na+ absorption in proximal bowel
counter-transport in exchange for H+ (equilibrating charge)
Na+ absorption in jejunum
co-transport with amino acids and monosaccharides
Na+ absorption in ileum
co-transport with Cl- (equilibrating charge)
Na+ absorption in colon
restricted movement through ion channels
2 types of secondary active transport of Cl-
co-transported with Na+ in ileum or exchanged with HCO3- in colon (both equilibrate charge)
how is K+ absorbed
passive diffusion via paracellular pathways into small intestine, and leaks out between cells in colon
fate of IC Na+
active transport into lateral IC spaces by Na+K+-ATPase in lateral plasma membrane, changing electrochemical gradient
why are Cl- and HCO3- transported into IC space
electrical potential created by Na+ transport
effect of high ion concentration in IC spaces
fluid around cells becomes hypertonic (high water potential)
effect of water on IC channels
distends, causing increase in hydrostatic pressure in cell; water also dragged into lateral intercellular spaces
fate of ions and water
move across basement membrane of epithelium and carried away by capillaries
where is Ca2+ absorbed
duodenum, ileum
effect of Ca2+ deficient diet on gut’s ability to absorb
increases
what stimulate absorption of Ca2+
vitamin D, parathyroid hormone
Ca2+ concentration gradient
low IC (100nM), high EC (1-3mM), allowing passive movement
how is Ca2+ carried across apical membrane
intestinal Ca2+-binding protein (IMcal) by facilitated diffusion, ion channel
purpose of Ca2+ and implications
IC signalling molecule, so must transport it in while maintaining low IC concentrations (prevent signalling cascade)
how is Ca2+ action as intracellular signal prevented
binds to calbindin in cytosol; dissociates when going to be pumped out
how is Ca2+ pumped across basolateral membrane into blood (higher concentration gradient)
primary active transport: Ca2+ATPase (PMCA) - high affinity - don’t need much Ca2+, low capacity - slow, maintaining very low concentrations of Ca2+ IC; secondary active transport: Na+/Ca2+ exchanger - low affinity, high capacity, requiring large Ca2+ concentrations
what is required for Ca2+ absorption
vitamin D (1,25-dihydroxy D3)
deficiency of vitamin D
rickets, osteoporosis
why is vitamin D taken up by enterocytes (3)
enhances Ca2+ transport through cytosol, increases calbindin levels, increases rate of extrusion across basolateral membrane by increasing level of Ca2+ATPase
functions of iron
electron donor and acceptor, used in oxygen transport and oxidative phosphorylation
iron toxicity
toxic in excess but no mechanism to actively excrete iron, so must be able to absorb quickly but able to limit absorption
how is iron present in diet
inorganic (Fe3+ - ferric/Fe2+ - ferrous), part of haem group (Hb, Mb, cytochromes)
what iron can be absorbed
Fe2+
why can’t Fe3+ be absorbed
forms insoluble salts with OH-, PO4 3-, HCO3-
what reduces Fe3+ to Fe2+
vitamin C
features of haem absorption
more readily absorbed, so dietary haem highly bioavailable; absorbed intact into enterocyte, via heme carrier protein 1 (HCP-1 via receptor-mediated endocytosis), Fe2+ liberated by Heme oxygenase
what catalyses reduction of Fe3+ to Fe2+ in duodenum
liberated by Heme oxygenase using duodenal cytochrome B
how is Fe2+ transported into cytosol
via divalent metal transporter 1 (DMT-1) - H+ coupled co-transporter
how does Fe2+ enter blood
binds to factors, carried to basolateral membrane, moves via ferroportin ion channel into blood
what converts Fe2+ to Fe3+ for transport around body
hephaestin (copper-dependent ferroxidase)
how does Fe3+ travel in blood
binds to apotransferrin and travels as transferrin
effect of hecidin on ferroportin function
suppresses so decreases iron absoprtion as can’t pump out into blood
how else does Fe3+ travel in blood
binds to apoferritin in cytosol to form ferritin micelle (Fe2+ oxidised and crystalises in protein shell) to trap Fe3+ in cell and make biologically inert
number of iron ions in single ferritin molecule
<4000
what happens in excess dietary iron consumption
produce more ferritin in cytosol to prevent it entering blood - stored as Fe3+
fate of ferritin in enterocytes if too much iron
irreversibly binds to iron in epithelial cells, so both unavaliable for transport into plasma, so are lost in intestinal lumen and excreted in faeces when enterocytes sloughed off
what are vitamins
organic compounds that cannot be manufactured by body but vital to metabolism
how are fat soluble vitamins (A,D,E,K) transported to brush border
micelles, except K+ which is actively taken up
what vitamins are there specific transport mechanisms for
vitamin C, folic acid, vitamin B1, vitamin B12
how are other vitamins taken up
passive diffusion
where is vitamin B12 stored
liver
effect of impaired B12 absoprtion
folate deficiency causing retarded maturation of red blood cells, causing pernicious anaemia
how is most B12 found in food
bound to proteins
how is denaturation of B12 by HCl in stomach avoided
binds to R protein (haptocorrin) released in saliva and parietal cells (R protein digested in duodenum)
what protein binds to vitamin B12 to prevent digestion in duodenum
binds to intrinsic factor (if no IF, no absorption of B12)
fate of B12/IF complex
binds to cubilin receptor, taken up in distal ileum by receptor-mediated endocytosis
where is B12/IF complex broken
mitochondria
fate of B12 in enterocyte, bloodstream and liver
binds to protein transcobalamin II (TCII), crosses basolateral membrane, travels to liver, uptaken by binding to TCII receptors, undergo proteolysis to break down TCII
