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Mineral Metabolism
Ca, P, Mg, Fe, Zn, I, Cu, Mn, Cr, Se
| Question | Answer |
|---|---|
| Ca distribution (& active compound) | 99% in bone structure as hydroxylapatite. 1% in/ex-cellular as a 2nd messenger, although small, the 1% has a big effect on signaling pathways |
| Ca functions (8) | 1)blood coagulation 2)neuromuscular contraction 3)membrane stability 4)enzyme activation 5)cell adhesion 6)neuronal transmission 7)signal transduction 8)triggers hormonal secretion |
| Ca 1. enzyme activation roles 2. neuronal transmission roles | cofactors for pancreatic lipase (lipid hydrolysis) and ATPase |
| Ca sources *significance w/ plants? | Best: milk/dairy (72% of intake) Good: seafood *plants contain Ca but also contain phytate and oxalate that celate Ca (-> deficiency) |
| Ca absorption & characteristics of the mechanisms of action | Active transport (ATP dep.)is most effective at low conc. of Ca through duod & jeju and is regulated by Vit D. Passive absorption is imp. at high conc. of Ca intake, occurs in SI, and is Vit D independent. Depends on amt. of Ca available & vit D status. |
| Ca absorption - enhancing & lowering factors | Enhance: compounds which chelate Ca into soluble forms (Lact,citr,lys,arg), vitD, sugar, low pH, Androgen. Lower: old age, female, stress(TH,Cort), fiber, high Ph, phytate, oxalate, high PO4 |
| Ca excretion | Major loss in urine Actively resorbed by the kidneys Dependent on vit D, PTH, Na/K/ATPase Kidney filters ~10g/day of Ca (99% resorbed, 100mg lost/day) |
| Ca excretion - enchancing & lowering factors | Enhance: CHO/Pro/Mg rich diet, Cort/TH/GH, PO4, caffeine. Lower: PTH, vit D, low serum Ca, metabolic alkalosis |
| Osteomalacia vs. Osteoporosis | o-malacia is a decrease in bone mineral (hydroxylapatite)& seen primarily in young people, O-porosis is a decrease in hydroxylapatite & extracellular matrix! & primarily seen in older people |
| 3 ways in which Phosphorous regulates bone metabolism | Control of 1.resorption vs. mineralization 2.collagen synthesis/ phosphorylation Indirect control of 3.calcium excretion & homeostasis |
| Phosphorous distribution & functions Intracelluar P >> Extracellular P | 85% in bone crystallized w/ Ca 15% ATP, nucleotides, phospholipids, phosphorylated metabolites (ex.G1P in muscle), phosphoproteins (phosphorylase targets), intracellular buffer |
| Phosphorous availability & mechanism of absorption | Readily released from most foods by intestinal alkaline phosphatase (removes P from substrate) Active transport w/ low intake (Na+dep.co- transporter,may be enhanced by vit D) Passive w/ high intake or vit D deficiency |
| Compounds which decrease P absorption | Phytate Fe++, Mg++, unsaturated fatty acids Al++ from antacids: chelates P & blocks absorption |
| Mineral A deficiency --> Mineral B deficiency Explain how a deficiency of Copper could cause deficiency of Iron | Cu transport protein, Ceruloplasmin, functions as ferrioxidase. Ferrioxidase oxidizes ferrous to ferric iron which binds to transferrin & is transported throughout the body. |
| Mineral deficiency --> Vitamin deficiency Explain how Zn deficiency can cause Folate deficiency | Conjugase(a Zn containing enzyme)is required for folate absorption. (the enzyme removes the polyglutamate residues on food folate resulting in monoglutamate which is the absorbed compound) |
| How do Zinc & Copper regulate the expression of metallothionien? | As Zn & Cu increase, they activate the nuclear metal binding protein, which binds to the metal response element present in the promoter region of metallothionein. This storage protein is responsie to Zn/Cu concentrations in the cell. |
| What roles do most minerals play? (except the electrolytes:Na,K,Cl) | Cofactors for proteins in which they play an enzymatic, structural, and/or transport role. |
| Wilson's disease | rare inherited disorder of copper accumulation and toxicity, caused by a defect in an enzyme that is part of the pathway of biliary excretion of excess copper -Can be effectively treated w/ Zn |
| Explain how Zinc may treat Wilson's disease | Zn induces metallothionein, which has a high affinity for Cu, and prevents the transfer of Cu into circulation. Intestinal cells (containing Cu-bound metallothionein) slough off every 6 days and are excreted in stool. |
| Magnesium distribution | 60% in bone (provides structure) 20% in muscle (neuromuscular transmission in skeletal muscle & modulates relaxation of smooth muscle:cardiac/digestive) 1% in serum (small yet plays large role) |
| Which minerals act on muscle? How? | Mg- modulates relaxation of smooth muscle Ca- modulates contraction of smooth muscle (influence on B.P.??) |
| Mg levels & Bone Formation | Low: increased PTH synthesis & release High: mimics Ca, suppresses Ca homeostasis, triggers calcitonin release for Ca resorption |
| Effects of High Mg & it mimicing Calcium | Mg may competitively bind to Ca binding sites to mimic or inhibit Ca-dependent responses. Mg displaces Ca in intracellular binding sites, thus raising the effective intracellular Ca concentration. |
| Mg & Intracellular monovalent cation concentrations | Influences in/extra cellular K+ balance especially in vascular & myocardial muscle. -Na/K/ATPase pump is Mg-dependent -intracellular K+ is maintained by Na/K/ATPase pump -if both are deficient, only Mg can restore K homeostasis *glucose is Mg dependen |
| Mg & Intracellular monovalent cation concentrations | Influences in/extra cellular K+ balance especially in vascular & myocardial muscle. -Na/K/ATPase pump is Mg-dependent -intracellular K+ is maintained by Na/K/ATPase pump -if both are deficient, only Mg can restore K homeostasis *glucose is Mg dependen |
| Mg & Cardiovascular disease | Observations show Mg may lower CVD risk by competing w/ Ca to maintain heart rhythm or widening the coronary arteries and improving blood flow. Mg deficiency has been seen in patients w/ chronic heart failure. |
| Mg deficiency | Risk mainly due to high excretion. = loss of muscle response, calcification of soft tissue, decreased B cell & antibody titers, diabetes connection |
| Mg toxicity | excess Mg possibly due to kidney failure symptoms- CNS depression, anesthesia, paralysis |
| Mg absorption & transport | ~30% is absorbed. evidence of both active and facilitated Transported largely as free ion or complexed w/ small molecules (lactate,citrate,lipoprotein surface) |
| Mg homeostasis & body pools | Primarily by excretion. Serum Mg is NOT under active control. Homeo depends on abs,excr,cell cation flux. 3 Pools based on turnover: 1)quick(excell) 2)medium(incell) 3)slow (skeletal matrix) |
| Mg deficiency risks | Diuretics, protein malnutrition, PTH disease, renal disease, DM, impaired GI function |
| Mg Assessment | DIFFICULT! serum Mg only reflects 1% of body Mg. Measure renal excretion after Mg IV load, a low excretion indicates a deficiency b/c of the increased retention. |
| Iron's function in oxygen transport, e' transport, and oxdiative enzymes | Heme-containing enzymes. Fe is bound to porphyrin ring whicn increases iron's redox and solubility properties. Porphyrin ring synthesis is dependent on B6! |
| Iron's role in free radical synthesis & degradation | Catalase (which breaks down hydrogen peroxide to water & oxygen) contains Fe heme. *also seen in glutathione peroxidase with Se |
| Iron's role in drug metabolism | Hydroxylation - cytochrome P450 & b5 use heme Fe or Fe-S centers to hydroxylate toxins for excretion by the body |
| What level does Fe metabolism regulation occur? | Translation - protein synthesis Central Dogma: occurs b/w mRNA and synthesis of a protein |
| Proteins of Iron Homeostasis | Transferrin- transfers Fe b/w cells (TfR syn: inversely r/t cell Fe) Ferritin- Fe storage(synthesis r/t cell Fe status) Iron Regulating Element Binding Protein- allows for Fe-dep translation, may be central regulator of Fe homeostasis |
| Transferrin | Class of iron binding proteins,Can bind 0,1,or 2 Fe3+, ~30% saturated, synthesized in liver, requires transferrin receptors. |
| How is Fe internalized by the cell? | Transferrin receports on cell membrane binds diferric transferrin & together are internalized. Fe is releaed into the cytosol. Tf & Tf receptor return to membrane and are reused. |
| How is so much Iron able to be stored? | Ferritin has a huge Fe binding capacity of 4500 Fe atoms per ferritin. Storage prevents oxidative damage from free Fe. It contains 24 subunits & makes Fe readily available when needed. |
| Idiopathic familial hemochromatosis | potential increase in body iron stores of 30-fold |
| thalassemias | inherited hypochromic anemia, defect in hemoglobin synthesis, increase in iron stores |
| sickle cell anemia | affects African Americans, defective hemoglobin is synthesized creating a moon shaped RBC |
| What is inflammation caused by iron deficiency? | drop in serum iron levels as a defense agaist invading organisms (bacteria, tumor cells?) may be an adaptive response |
| What is porphyrias? | a defect in heme formation |
| Which mineral is required for testosterone synthesis? | Zinc |
| Zinc Functions | cofactor in >100 enzymes. CHO, protein, energy metabolism. DNA/RNA stabilization, transcription factor, testosterone synthesis. |
| Zn absorption | increased by citrate by increasing Zn solubility. decreased by phtate and fiber. bound to albumin etc. in serum |
| Zn excretion routes | 1. via pancreatic enzymes 2. sloughed w/ mucosal cell bound to metallothioneine into intestine and feces |
| Zn transfer from mucosa to blood has competition from which other minterals? | Cu++, Fe++, Fe+++ |
| Symptoms of Zinc deficiency | Growth retardation(loss of hGH), Impaired male dev., Acrodermatitis, Loss of taste & smell, Decreased wound healing (collagenase, DNA seq. in steroid receptors), Decr. immunity, Impaired embryogenesis |
| Why does Zinc deficiency cause impaired embryogenesis? | Lack of cell differentation. deficient Zinc fingers for vitamin A nuclear receptors. (vit A is vital for cell differentiation) |
| Copper functions | Enzymatic cofactor in oxygenases (+OH via oxygen). Maintains immune functions. Stimulates angiogenesis. Inactivates neuro-active amines. Enhances antiinflammatory drugs? |
| Cu-related enzymes | cytochrome oxidase-last protein in e transfer chain. SOD. LOX collagen synthesis. Tyrosinase- melanin syn. Ceruloplasmin- serum Cu transporter. Inactivates histamin & tyramine. Makes catecholamine neurotransmitters. |
| Cu absorption | decreased by fiber and zinc. increased by amino acids. energy-dependent and regulated. binds wth metallothionein in mucosa. |
| Cu metabolism | Bound to metallothionein or transported in blood and binds to albumin or transcuprein then sent to the liver. Cu is used for enzymes, attached to ceruloplasmin & sent to tissues or excreted through bile. |
| Cu toxicity | RARE, mostly accidental poisoning. treated w/ Zn to compete w/ Cu absorption. possible inborn error of metabolism called Wilson's Disease. |
| Cu deficiency | Rare* possibly w/ kidney dialysis or premature infants on TPN. Menke's Disease: inborn error-Cu accumulates in blood. mental retardation, brittle hair, death by 3 |
| Cu deficiency symptoms vs. reason-anemia-connective tissue dysfunction-lack of myelination-lack of pigmentation-depressed immunity | -impaired iron mobilization-impaired collagen synthesis-? also w/ B12 deficiency-lack of tyrosine/melanin synthesis-? |
| Iodine function | Component of thyroid hormone T3 & T4- a regulator of metabolism and gene expression (RAR/RXR) |
| Iodine absorption/transport | readily converted to anion in the gut, absorbed by active transport Na/K/ATPasemost serum iodine is cleared by thyroid gland |
| Synthesis of Thyroid Hormones | made by iodine's posttranslational modification of tyrosine. DIT+MIT->T3 tri-iodothyronine (very active)DIT+DIT->T4 thyroxin*T3 is 3x more potent than T4*iodination is very rapid! & stored in thyroid gland follicle (95% of iodine storage) |
| Release of Thyroid Hormones | Thyroglobulin is recalled from follicle and merges w/ lysosome rich proteases which release T3 and T4 to enter the blood. MIT & DIT are released, deiodinized, and iodine is reused. |
| What factor and hormone are involved with tyroid hormone signal regulation? | TRF: thyroid-releasing factor (in hypothalmus)TSH: throid-stimulating hormone (in pituitary) |
| Which thyroid hormones (T3/T4) are favored when serum iodine is restricted and in excess?How are the thyroid hormones transported? | restrited I = T3 synthesis is favoredexcess I = T4 synthesis is favoredtransthyretin (+RBP/vit A) |
| What must be done for optimal activity of thyroid hormone? | T4 must be converted to T3 via deiodinase which is Selenium dependent. T3 then binds one of several nuclear thyroid homone receptors to turn on target genes specific for that cell type. |
| What physiological effects does thyroid hormone have? | Enhances BMR, affects macronutrient synthesis, uncouples oxidative phosphorylation at high concentrations, may inhibit phosphodiesterase, and reduces serum lipids (FA & chol.) |
| Iodine deficiency *defects in thyroid hormone not = to iodine deficiency* | GOITER- lack of I causes inability to synthesize T3/4. TSH is released anyway causing hyperplasia of thyroid gland. huge neck bulge!CRETINISM- mental defect w/ severe muscle spasms, deaf mutism, short stature |
| True or False? There is no evidence that Chromium is an enzymatic cofactor. | True - Mechanism for chromium usage is still unknown. Determined essential in 1959. |
| Chromium deficiency | Seen in long term TPN patients. Loss of glucose homeostasis & abnormal lipid metabolism. Hyperlipidemia - affect on HMGCoA reductase?Glucose intolerance restored by Brewer's yeast, not w/ Torula's yeast. |
| Cr absorption/metabolism | 1-2% efficiency. lowest serum concentration of all micronutrients. travels on transferrin like Fe but also binds albumin, lactate, citrte, etc. Hair is greatest storage site. |
| True or False? Aluminum is essential. | False - relatively biologically inert, except at toxic doses. Important detrimental interactions w/ other nutrients. |
| Al toxicity/pharmaceutical applications | Toxicity in patients taking Al-containing antacids. Causes osteomalacia, anemia, alzheimers. Used as a phosphate binder to treat hyperphosphatemia in renal failure patients. Was a contaminant of TPN protein source (casein hydrolysates) |
| Al & Osteomalacia | 1st seen in TPN patients. Al accumulates in bone, particularly at mineralization boundary. Leads to frequent bone fractures & severe bone pain. Removes Pi from bone, blocks mineralization & intestinal uptake of Pi when given orally. |
| Al & microcytic hypochromic anemia | Competes w/ iron absorption in the mucosa. Binds ferritin, & thus depletes intracellular Fe stores and interferes with Fe mobilization. |
| Al & Alzheimer's | Seen in popular press but largely disproven. Al interferes w/ Ca-dependent actions within neurons. |
| What makes Al so toxic?? | Difficult to excrete!! Only 1% of body stores is excreted in urine. Al continues to build up over time. |
| Selenium functions | Protects agains oxidative damage from free radicals. (ie glutathione peroxidase)Participates in thyroid hormone metabolism! |
| Selenium deficiency | Keshan's disease-arrhythmia, cardiomyopathy, heart enlargement, & loss of heart tissue |
| Se metabolism | 50-90% absorbedSelenomethionine absorbed better than inorganic Se. Excreted in urine. |
Created by:
sbradley1
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