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Trace Elements Reed A Berger MD Visiting Clinical Professor in Nutrition Trace Elements -a naturally occurring, homogeneous, inorganic substance required in humans in amounts less than 100 mg/day 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 AA’s 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… Absorption, Transport, Excretion -some absorption from the stomach, but most in the small intestine -absorption varies—it decreases with increased intake 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 -secreted from the liver as a component of bile -once in the GI tract, it becomes part of the body’s pool and is reabsorbed or excreted depending on the body’s 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 -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 RDA and Sources -see handout 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 degeneration>>>death -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 Menke’s 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 Menke’s cont’d -there is accumulation of copper in the intestinal mucosa even though copper and ceruloplasmin levels are very low -transient improvement with parenteral copper -***decreased plasma copper levels are also seen in malabsorptive diseases, celiac sprue, tropical sprue, proteinlosing enteropathies, and nephrotic syndrome Toxicity -increased copper levels seen during pregnancy and in women on OCP’s, 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 -***Wilson’s disease: accumulation of excessive copper in the body tissue as the result of a genetic deficiency in the liver synthesis of ceruloplasmin 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 -it’s only function is related to thyroid hormone 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 Deficiency -goiter—enlargement of the thyroid gland -deficiency may be absolute—in areas of deficiency, or relative—adolescence, pregnancy, lactation -goiters are more prevalent in women and with increased age -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: cretinism—mental deficiency, spastic diplegia, quadriplegia, deaf mutism, dysarthria, shuffling gait, short stature, hypothyroidism Toxicity -iodine has wide margin of safety -goiter usually occurs with excess intake>need Chromium--Functions -required for normal lipid and CHO metabolism and for the fxn of insulin -?can supplementation raise HDL Absorption and Excretion -10-25% absorption in its trivalent form -amount absorbed remains constant at dietary intakes >40 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 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 Cobalt -most stored with vitamin B12 -component of B12—cobalamin -essential for maturation of RBC’s and normal function of all cells 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 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 deficient—happens in vegetarians Deficiency -related to vit B12 deficiency -**macrocytic anemia -genetic defect: pernicious anemia -tx: massive doses -more in the vitamin lecture Toxicity -polycythemia -hyperplasia of BM -reticulocytosis -increased blood volume 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 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 RBC’s or selenium levels in whole blood or urine -RBC selenium is an indicator of longterm status Deficiency -rare -Keshan Dz or Kashin-Beck Dz -long term TPN, cancer, CF 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 SE’s -Deficiency: increased risk with coexisting copper deficiency, TPN Silicon, Vanadium, Arsenic, Boron -see handouts -will not be on the exam!!!