Transported as free Ca2 or bound to albumin Increases Ca and Pi absorption

Transported as free ca2 or bound to albumin increases

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Transported as free Ca2+ or bound to albumin Increases Ca (and Pi) absorption - 1,25(OH) 2 D 3 binds to VDR & stimulates expression of TRPV6 & PMCA1b VDR binds to 1,25(OH) 2 D 3 and forms heterodimer with RXR 1,25(OH) 2 D 3 -RXR complex binds to VDRE & stimulates tx of Ca handling genes TRPV6, calbindin &
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4 PMCA1b - Ca transport is a saturable process comprised of three 1,25(OH) 2 D 3 regulated steps: Entry of Ca through the membrane channel via TRPV6, located in the apical membrane of the intestinal epithelium Binding to the Ca binding protein, calbindin which shuttles Ca through the enterocyte § Calbindin expression stimulated by 1,25(OH) 2 D 3 ; inhibited by vit D def - Export of Ca across the basolateral membrane by PMCA1b Maintains Ca levels with PTH 1. Parathyroid gland senses low Ca lvls in blood & signals PTH release 2. PTH stimulates kidney to o Ca reabsorption o Stimulate renal 1- hydroxylase to convert 25(OH) 2 D 3 to 1,25(OH) 2 D 3 (calcitriol) 3. blood calcitriol stimulates Ca absorption in intestine - Calcitonin acts opposite to PTH: o Inhibits osteoclast resorption to lower Ca & PO4 Absorption enhanced by: Vit D, sugars, EtOH Inhibited by phytates, oxalates Dietary Na is the key dietary factor influencing urinary Ca loss
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5 Selenium largest SE mass in muscle; total body Se = 30mg Food forms: Plants- selenomethionine & methionine Animals- selenocysteine & cysteine - Selenocysteine (SEC) = 21 st AA, Se takes place of S in Cys; relies on independent Sec insertion machinery to coding in the genetic code - Unknown fxns, but participate in AOX & anabolic processes o Selenoprotein P (SELP) accounts for 80% of plasma Se o Glutathione peroxidase- protects thyroid from ROS o Iodothyronine deiodinases- converts T4 to T3 o Thioredoxin reductase- act as AOX as e- donors (reducing agent) o SELW implicated in white muscle disease 55ug/d Se def & toxicity caused by inadequate/xs intake directly caused by Se in soil: Keshan disease (def) à cardiomyopathy Kashin Beck disease Occurs where low Se in soil à affects cartilage Myxedematous Cretinism à thyroid enlargement caused by Se and iodine **in def, Se absorption does not increase TOXICITY = selenosis UL = 400ug/d - Imported via luminal & basolateral inorganic Se transporters (none described yet) - Methylselenol = major excretory form in urine - Plasma Se (recent diet) - RBC Se (long term) Iodine Iodine – element; free iodine is a gas Iodide- ionic form; soluble in water Iodate used in fortification - Only fxn: syn of thyroid hormones by the thyroid gland o Thyroxine (T4) & Triiodothyronine (T3) o Utilizes Tyr - Hormone fxns via binding to RXR heterodimer in nucleus: o Bone maturation o BMR o Neuronal cell & bone growth in fetuses - *Several tissues deiodinate T4 to T3 via 5’-deiodinase which requires Se - *Glutathione peroxidase (requires Se) protects thyroid 200ug/d Common deficiency due to lack of I in soils - Goiter: ↓plasma I = ↓ hormone syn = ↑TSH Ø ↑thyroid cell # Ø ↑thyroid cell size Ø Enlarged thyroid gland - Pregnancy ↑ thyroid hormone production by 50% o Severe def during pregnancy à cretinism - Imported via Na+/I- symporter as iodide -
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  • Spring '14
  • Knutson,MitchellD
  • Vitamin, Vitamin B12, enterocytes

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