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Trace Elements

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Title: Trace Elements


1
Trace Elements
  • Reed A Berger MD
  • Visiting Clinical Professor in Nutrition

2
Trace Elements
  • -a naturally occurring, homogeneous, inorganic
    substance required in humans in amounts less than
    100 mg/day

3
Copper
  • -found in the liver, brain, heart, kidneys, and
    muscle
  • -about 90 of copper in the plasma is in the form
    of ceruloplasmin
  • -the rest is bound to albumin, transcuprein, and
    AAs

4
Functions
  • -component of many enzymes
  • -oxidation of Fe prior to transport in the plasma
  • -cross-linking of collagen
  • -mitochondrial energy production, protection from
    oxidants, etc

5
Absorption, Transport, Excretion
  • -some absorption from the stomach, but most in
    the small intestine
  • -absorption variesit decreases with increased
    intake

6
Metabolism
  • -for short term transport to the liver copper is
    carried primarily by albumin
  • -copper-albumin complex acts as a temporary
    storage site for copper
  • -in the liver, metallothionein is the storage
    site
  • -ceruloplasmin is the storage site in the plasma
    and cells

7
  • -secreted from the liver as a component of bile
  • -once in the GI tract, it becomes part of the
    bodys pool and is reabsorbed or excreted
    depending on the bodys need
  • -biliary excretion increases in response to
    copper overload
  • -small amts of copper are present in the urine,
    sweat, and menstrual blood
  • -can be conserved by the kidney for reabsorption

8
  • -unabsorbed copper is in the feces
  • -in high levels, zinc can induce copper
    deficiency by stimulating intestinal cells to
    produce more metallothionein which binds copper
    more avidly than zinc and then is exfoliated with
    the intestinal cells
  • -fiber and phytate do not adversely effect copper
    absorption

9
RDA and Sources
  • -see handout

10
Deficiency
  • -decrease in serum copper and ceruloplasmin
    levels are seen
  • -neutropenia, leukopenia,bone demineralization
  • -subperiosteal hemorrhages, hair and skin
    depigmentation, defective elastin formation
  • -failure of erythropoiesis, cerebral and
    cerebellar degenerationgtgtgtdeath

11
  • -neutropenia, leukopenia are the best early
    indicators in children
  • -because it is stored in the liver, deficiency
    takes a long time to develop
  • -bone changes such as osteoporosis, soft tissue
    calcification can occur with prolonged TPN

12
Menkes disease
  • -sex-linked recessive defect that results in
    copper malabsorption, increased urinary loss, and
    abnormal intracellular copper distribution
  • -affected infants retarded growth, defective
    keratinization and pigmentation of hair,
    hypothermia, degenerative changes of the aorta,
    mental deterioration, abnormalities of the
    metaphyses of long bones
  • -all of the above is due to interference with
    collagen and elastin cross-linking

13
Menkes contd
  • -there is accumulation of copper in the
    intestinal mucosa even though copper and
    ceruloplasmin levels are very low
  • -transient improvement with parenteral copper

14
  • -decreased plasma copper levels are also seen
    in malabsorptive diseases, celiac sprue, tropical
    sprue, protein-losing enteropathies, and
    nephrotic syndrome

15
Toxicity
  • -increased copper levels seen during pregnancy
    and in women on OCPs, those with acute and
    chronic infections, pts with liver disease
  • -any liver disease that interferes with bile
    excretion (primary biliary cirrhosis) and
    mechanical obstruction causes increases in liver
    copper
  • -Wilsons disease accumulation of excessive
    copper in the body tissue as the result of a
    genetic deficiency in the liver synthesis of
    ceruloplasmin

16
Iodine
  • -body normally has 20-30 mg of iodine and more
    than 75 is in the thyroid gland
  • -the rest is in the mammary gland, gastric
    mucosa, and blood
  • -its only function is related to thyroid hormone

17
Absorption and Excretion
  • -iodine is absorbed in the form of iodide
  • -occurs both as free and protein-bound iodine in
    circulation
  • -iodine is stored in the thyroid where it is used
    for the synthesis of T3 and T4
  • -the hormone is degraded in target cells and in
    the liver and the iodine is conserved if needed
  • -excretion is primarily via urine
  • -small amts from bile are excreted in the feces

18
Deficiency
  • -goiterenlargement of the thyroid gland
  • -deficiency may be absolutein areas of
    deficiency, or relativeadolescence, pregnancy,
    lactation
  • -goiters are more prevalent in women and with
    increased age

19
  • -goitrogens occurring naturally in foods can
    cause goiter by blocking absorption or
    utilization of iodine (cabbage, turnips, peanuts,
    soybeans)
  • -severe deficiency during gestation and early
    postnatal growth cretinismmental deficiency,
    spastic diplegia, quadriplegia, deaf mutism,
    dysarthria, shuffling gait, short stature,
    hypothyroidism

20
Toxicity
  • -iodine has wide margin of safety
  • -goiter usually occurs with excess intakegtneed

21
Chromium--Functions
  • -required for normal lipid and CHO metabolism and
    for the fxn of insulin
  • -?can supplementation raise HDL

22
Absorption and Excretion
  • -10-25 absorption in its trivalent form
  • -amount absorbed remains constant at dietary
    intakes gt40 ug (micrograms) at which point
    excretion in urine is proportional to intake
  • -increased intake of simple sugar, strenuous
    exercise, or physical trauma also increase
    urinary excretion
  • -both chromium and Fe are carried by Tf, however
    albumin can also assume this role

23
Deficiency
  • -altered CHO metabolism, impaired glucose
    tolerance, glycosuria, fasting hyperglycemia,
    increased insulin levels and decreased insulin
    binding
  • -impaired growth, peripheral neuropathy, negative
    nitrogen balance
  • -increased chromium losses in stress
  • -hyperglycemia and wt loss reverse with IV
    supplementation in TPN

24
Cobalt
  • -most stored with vitamin B12
  • -component of B12cobalamin
  • -essential for maturation of RBCs and normal
    function of all cells

25
Absorption and Excretion
  • -shared with Fe
  • -absorption is increased in pts with deficient Fe
    intake, portal cirrhosis with Fe overload, and
    hemochromatosis
  • -excretion is mainly thru the urine
  • -small amts in feces, hair, sweat

26
Sources and Intakes
  • -microorganisms are able to synthesize B12
  • -humans must obtain B12 and cobalt from animal
    foods such as organ and muscle meat
  • -takes a long time to become deficienthappens
    in vegetarians

27
Deficiency
  • -related to vit B12 deficiency
  • -macrocytic anemia
  • -genetic defect pernicious anemia
  • -tx massive doses
  • -more in the vitamin lecture

28
Toxicity
  • -polycythemia
  • -hyperplasia of BM
  • -reticulocytosis
  • -increased blood volume

29
Selenium
  • -glutathione peroxidase
  • -acts with other antioxidants and free radical
    scavengers
  • -overlaps with vit E for antioxidant effects
  • -fxn with vit E to protect cell and organelle
    membranes from oxidative damage

30
Absorption and Excretion
  • -upper segment of the small intestine
  • -increased absorption with deficiency
  • -status is measured by measuring selenium or
    glutathione peroxidase in plasma, platelets, and
    RBCs or selenium levels in whole blood or urine
  • -RBC selenium is an indicator of long-term status

31
Deficiency
  • -rare
  • -Keshan Dz or Kashin-Beck Dz
  • -long term TPN, cancer, CF

32
Molybendum
  • -relationship with copper and sulfate
  • -cofactor of many enzymes involved in the
    catabolism of sulfur AA, purines and pyridines
  • -Toxicity gout-like syndrome, reproductive SEs
  • -Deficiency increased risk with co-existing
    copper deficiency, TPN

33
Silicon, Vanadium, Arsenic, Boron
  • -see handouts
  • -will not be on the exam!!!
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