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NUTR 3210 > Lecture 14 - micronutrients part 1 > Flashcards

Lecture 14 - micronutrients part 1 Flashcards

1
Q

What is group I?

A

micronutrients that control type II steroid hormone receptors and have major global health implications
iodine, Vit A, Vit D, calcium, Vit K, phosphorus and fluoride

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2
Q

What is Group II?

A

micronutrients that have a role in oxidant defense
Vit E, Selenium, Vit C, Niacin, Riboflavin, Copper, Zinc, manganese

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3
Q

What is Group III?

A

Micronutrients that act as enzyme cofactors
thiamin, niacin, riboflavin, Vit B6, folate, Vit B12, Biotin, Pantothenic acid

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4
Q

What is Group IV?

A

Iron, Copper, and zinc-related divalent cations

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5
Q

What does bioactive mean?

A

they can interact with eachother and cause an output, a functional form

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6
Q

Do all of the group I micronutrients act directly on steroid hormone receptors?

A

No, only the bioactive forms of vit a, it d and iodine

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7
Q

What is iodine used to make?

A

T3 hormone, which regulates synthesis of proteins that control a persons basal metabolic rate

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8
Q

What is Vit A used to make?

A

Vit A precursors are converted to retinoids, which regulate night vision, epithelial differentiation and gene expression

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9
Q

What is Vit D used to make?

A

Vit D precursors are converted to calcitriol, which regulates calcium levels in the body

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10
Q

What is a steroid hormone receptor?

A

intracellular protein receptors that need to bind a ligand to become a functional (active) transcription factor

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11
Q

What are the two types of steroid hormone receptors?

A

Type 1 and Type 2

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12
Q

What is a Type 1 steroid hormone receptor?

A
  • cytosolic
  • respond to steroid hormones like estrogen, testosterone, progesterone, glucocorticoids, and mineralcorticoids
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13
Q

What is a type 2 steroid hormone receptor?

A
  • nuclear
  • respond to steroid and non-steroid ligands, like thyroid hormone, retinoic acid and calcitriol
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14
Q

Is iodine high in most foods?

A

No, iodine content of most foods is low

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15
Q

Is iodine organic or inorganic

A

inorganic

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16
Q

Is iodine water soluble?

A

iodine is highly water soluble

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17
Q

Where is iodine found in higher concentrations?

A

in coastal populations compared to mountainous regions, seafood has high concentrations, especially sea greens

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18
Q

What is fortification?

A

to increase the nutritional value of food by adding vitamins or minerals

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19
Q

How is iodine consumed in north america?

A

through salt fortified with potassium iodine

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20
Q

How can iodine be found in the body?

A

dietary iodine can be bound to AA or found free

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21
Q

What is iodine converted to?

A

in GI tract, iodine (I) is rapidly converted to iodine (I-) and absorbed

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22
Q

Where is iodine absorbed?

A

in the stomach, a bit in the small intestine

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23
Q

What does iodide do once it is absorbed in the stomach?

A

in the blood, free I- circulations and can enter all tissues (most accumulates in the thyroid gland)

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24
Q

How much of our bodies iodine is found in the thyroid gland?

A

70-80%

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25
Q

What is uptake of I- in the thyroid gland mediated by?

A

active transport system known as the Na+/I- symporter

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26
Q

NIS

A

Na+/I- symporter

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27
Q

Do tissues rely on iodine itself?

A

no, tissues actually rely on the thyroid hormones made by iodine, T3 and T4

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28
Q

What is the process of making T3 and T4 from iodide?

A
  1. dietary iodide is absorbed from GIT into the blood and is taken to the thyroid
  2. iodide enters the thyroid through NIS (active transporter)
  3. iodide enters the colloid of a thyroid cell and it is quickly oxidized to form a free radical I’
  4. iodide radical attacks the Tyr residues in THG un the colloid, which causes a cross-linking between tyrosine residues
  5. thyroid cells proteases hydrolyze THG, releasing fragments that correspond to T3 and T4 hormones
    - note: there is less T3 produced, and more T4 produced
  6. The T4 produced travels (in blood through carrier proteins) to the liver for storage, where it can be converted to T3 through 5’ deiodinase (selenoprotein), the T3 made there is then used for function in the body
  7. The T3 made in the thyroid is directly used for function in the body
  8. the hypothalamus sense low T3 and sends neural signals to the pituitary to cause the release of TSH
  9. TSH travels to the thyroid to stimulate the production of more T3
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29
Q

What is the function of the T3 hormone?

A

regulates metabolic rate and growth in many tissues through interaction with the thyroid hormone receptor

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30
Q

Is T3’s half-life longer than T4?

A

T3 half-life <T4

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31
Q

What does T3 interact with?

A

Thyroid hormone receptor (THR)

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32
Q

THR

A

thyroid hormone receptor

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33
Q

What hormone regulates T3 and T4 production?

A

TSH

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34
Q

How much T3 vs T4 is there in the blood?

A

50 x more T4 in the blood than T3, but T3 is 100 x more potent

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35
Q

THG?

A

thyroglobulin protein

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36
Q

Where is THG produced?

A

in the thyroid cell (nucleus) and then released in the colloid (lumen), THG is a tyrosine rich protein, it is exocytosed into the colloid

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37
Q

What does T4 and T3 stand for?

A

T4 - thyroxine
T3 - Triiodithyronine

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38
Q

What is the function of thyroid hormones?

A

influence how your body stores and uses energy (effects metabolism)

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39
Q

What are the 9 things thyroid hormones control?

A
  1. breathing
  2. heart function
  3. nervous system function
  4. body temp
  5. cholesterol level
  6. energy balance
  7. brain development
  8. moisture in the skin
  9. menstruation
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40
Q

What are some characteristics of the T3 and T4 hormones?

A
  • T3 and T4 are lipophilic (can easily cross plasma membranes)
  • T4 is converted into T3 in various tissues (primarily in the liver)
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41
Q

What does T3 bind to?

A

in tissues, T3 binds to THR, which then binds to response elements in the promoter regions of DNA to activates gene expression (mRNA)

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42
Q

When T3 indirectly activates gene expression, what do the induced genes effect?

A
  • ATPases (pump Na+ and Ca2+ out of cells) which increases metabolic rate
    (Na+ muscle contraction, neuron firing) (Ca2+ signalling events)
  • growth hormone (anabolic effects)
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43
Q

What happens when there is an iodine deficiency?

A
  • when T3 levels are low, the pituitary gland releases TSH to turn iodide into T3
  • when iodine is deficient, the thyroid is still being stimulated by TSH to make hormones, but it can’t, this causes hyperplasia (increase in cell number), and hypertrophy (increase in cell size)
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44
Q

What are the health effects of iodine deficiency?

A

goitre (in adults) -> thyroid enlargement
- mild goitres can be treated with iodine supplements
- if left untreated, they become thyroid cancer
cretinism -> When iodine levels are low in the mother, the fetus doesn’t develop properly
- growth and development abnormalities
- irreversible

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45
Q

What is vitamin A referring to?

A

a group of compounds known as retinoids

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46
Q

What are major forms of vitamin A in the body?

A

retinol, retinal, retinoic acid and retinyl ester

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47
Q

What are carotenes?

A

precursors for vitamin A, they are a type of carotenoid, which are pigments produced in plants

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48
Q

What are animal livers rich in?

A

retinol and retinyl ester

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49
Q

What are orange and dark green vegetables rich in?

A

beta-carotene

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50
Q

What is a retinyl ester composed of?

A

retinol and FA

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51
Q

What do retinyl esterases do?

A

cleave the FA from the retinol

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52
Q

How is vitamin A digested and absorbed steps?

A
  1. a fat droplet from the stomach containing retinyl esters and beta carotene are acted on by pancreatic retinyl esterase and retinol and beta carotene are absorbed as a micelle through passive diffusion into an intestinal mucosal cell
  2. beta carotene can either go straight to the chylomicron or can form retinal through 15,15’ DO which then forms retinol
  3. this retinol becomes retinyl palmitate through the palmityl CoA enzyme
  4. the retinyl palmitate is then packaged in a chylomicron and goes into the lymphatic circulation
  5. the chylomicron then gets rid of TAGs to become a chylomicron remnant and the contents of it are absorbed in the liver
  6. in the liver, beta carotene can be stored there or can be packaged into a VLDL and sent out into circulation to go to adipose tissue (hypercarotenosis)
  7. in the liver, retinyl palmitate can be stored or can become retinol through retinyl esterase when it is needed for vitamin A
  8. once it becomes retinol, it combines with RBP to form retinol-RBP and travels through the blood to be recognized by a receptor on the target tissue
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53
Q

RBP

A

retinol binding protein

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54
Q

What is taken into circulation when vit A is low?

A

retinol-RBP

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55
Q

What is used to check if there is a vitamin A deficiency?

A

retinol-RBP

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56
Q

What do low levels of retinol-RBP stimulate?

A

hepatic retinyl esterase

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57
Q

What is the ability of vitamin A and beta carotene to pass through membranes?

A

vitamin A and beta carotene are lipophillic, therefore they are handled like other lipids

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58
Q

What are the two fates of beta carotene in the liver?

A

depending on the vit a status of a person, beta carotene will be either
1. incorporated into chylomicrons “as is”
2. or converted into retinyl ester in the intestinal cells and then incorporated into chylomicrons

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59
Q

Where are retinyl esters stored?

A

in hepatic stellate cells until needed

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60
Q

What happens when retinyl esters are needed?

A

liver retinyl esterase removes the FA releasing retinol which binds to retinol-binding protein (RBP) and secreted into blood, liver RBP synthesis depends on persons vit a status

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61
Q

RA

A

retinoic acid

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62
Q

What does retinol-RBP do?

A

brings retinol to cells, and can then be converted into RA

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63
Q

What is the function of RA?

A

goes to nucleus and binds and activates both the RAR and the RXR TF’s
these complexes homo and hetero dimerize with other nuclear hormone receptors (NHR) creating a huge number of possible combination of TF’s which allows the regulation of gene expression

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64
Q

RAR

A

retinoic acid receptor

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65
Q

RXR

A

retinoid X receptor

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66
Q

NHR

A

nuclear hormone receptor

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67
Q

Where are stem cells located?

A

rapidly dividing stem cells are in all epithelial tissues

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68
Q

What happens when there is a vitamin A deficiency in epithelial differentiation steps?

A

When vitamin A is present:
stem cells have normal cell differentiation then columnar epithelium secretes mucus and keratinization, some cells are sloughed off which results in cell death

When vitamin A is deficient:
stem cells continue to rapidly divide and cause poor differentiated function, in the epithelial cells, there is keratinization, but little mucus secretion, there is not enough mucus to form a good protective layer, so viruses and bacteria can penetrate

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69
Q

What is an issue with stem cells and vitamin a deficiency?

A

keratin is a major problem in all epithelial cells whose expression is regulated by retinoic acid

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70
Q

What does vit A deficiency in stem cells cause in various parts of the body?

A

cornea: xeropthalmia
lungs: respiratory infections
GI tract: diarrhea
skin: folliculosis

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71
Q

What are the 5 consequences of vitamin A deficiency?

A
  1. night blindness: reversible, one of the first signs of vit a deficiency, associated with bitot spots, a buildup of keratin debris in the conjunctiva of the eye
  2. impaired epithelial cell differentiation: can cause permanent blindness and life-threatening infections
  3. impaired growth (growth hormone not produced): impacts bone development, tooth decay etc.
  4. impaired fertility: decreased sperm formation, fetal resorption (early death of the embryo)
  5. fetal development defects: birth defects due to loss of control of differentiation, can occur with too little or too much vit a
72
Q

RAE

A

retinol activity equivalents

73
Q

What is RAE?

A

RAE accounts for differences in the biological activity of various carotenoids

74
Q

Why is there no UL for beta carotene?

A

carotenoids prevent deficiency but don’t cause toxicity, will just be stored if there are enough

75
Q

What occurs during vitamin A dietary toxicity?

A

most severe consequence is liver cell death
- retinyl ester are stored in the stellate cells of the liver and with excess vit a intake, the cells reach capacity, raw vit a spills out and the local hepatocytes become damaged and die

76
Q

What can excessive intake of beta carotene cause?

A

hypercarotenosis (skin turns yellow-orange)

77
Q

What does the bioactive form of vit D act as?

A

a hormone, works with other hormones such as parathyroid and calcitonin

78
Q

Where is the bioactive form of vit D made?

A

liver only

79
Q

What are the five forms of vitamin D sources

A
  1. natural plant sources (provitamin D2)
  2. natural animal sources (provitamin D3)
  3. sunlight
  4. supplementation
  5. fortification
80
Q

What is an example of a natural plant source that provides vitamin D

A

shitake mushrooms

81
Q

What is an example of a natural animal source that provides vitamin D

A

fish, fish liver oils

82
Q

Is vitamin D very active in plants?

A

no, so plant sources are not a very good source of vitamin D

83
Q

Which provitamin D2 is more bioactive?

A

(D3) cholecalciferol is more bioactive than (D2) ergocalciferol

84
Q

How is vitamin D made in the skin?

A

vit D3 is made in the skin from 7-D
7-dehydrocholesterol (7-D) is converted to (D3) cholecalciferol by sunlight (UVB and infrared), this occurs in the sebaceous glands of the skin

85
Q

How does vitamin D3 circulate around the body?

A

D3 binds to the vit D binding protein (DBP) and circulates throughout the body

86
Q

How does melanin slow down vit D3 production?

A

melanin in the epidermis absorbs UV rays, which slows down vit D3 production, part of the problem for Vit D deficiencies over time (migrating populations)

87
Q

What bioactive form of vitamin D is used in supplements?

A

Vit D3

88
Q

Where is fortification of vitamin d found?

A

milk and margarine, insufficient for health if this is a persons only source of vit D3

89
Q

Is there a risk of vitamin D toxicity from the sun?

A

no

90
Q

What are the steps to vitamin D3 production in the skin?

A
  1. UV rays hit the skin and convert 7-D to vit D3
  2. vit D3 has two fates
    - bind to DBP and go into the adipose tissue for storage, eventually goes to liver
    - bind to DBP and go directly into the liver for conversion
91
Q

What are the steps to vitamin D3 production in the diet?

A
  1. vit D3 is absorbed passively in the ileum (not very efficient)
  2. vit D3 is incorporated into chylomicrons and eventually ends up in the liver for conversion
92
Q

Is there a difference between sun derived vitamin D3 and diet-derived vitamin D3?

A

no

93
Q

What is vitamin D3 converted to in the liver?

A

Vit D3 ->(25-hydroxylase) 25-OH

94
Q

What are the steps to vitamin D3 conversion in the liver?

A
  1. in the liver, the 25th carbon on vitamin D3 is hydroxylated to form 25-OH D3 (inactive molecule) by the25-hydroxylase enzyme
  2. once produced, 25-OH D3 is secreted into blood bound to DBP (this corresponds to the largest pool of 25-OH D3 in the body
95
Q

what type of enzyme is 25-hydroxylase?

A

a cytochrome p450 enzyme

96
Q

What is a sign of vitamin D3 deficiency?

A

if 25-OH D3 levels in the blood are low

97
Q

What happens with regards to vitamin D when calcium levels are low in the body?

A

25-OH D3 will be converted to an active molecule

98
Q

Does vitamin D regulate calcium homeostasis?

A

yes

99
Q

What are the steps to forming the active form of vitamin D3 after D3 is converted to 25-Oh D3 in the liver?

A
  1. 25-OH D3 binds to DBP and circulates around the blood
  2. it eventually enters the kidney where 25-OH D3 enters
  3. low Ca2+ levels in blood plasma activate the parathyroid to release PTH (parathyroid hormone) promotes uptake of 25-OH D3/DBP complex into the kidney which enters the kidney and turns 25-OH D3 into 1,25-OH2 vit D3 (calcitriol) by the enzyme 1-hydroxylase
  4. 1,25-OH2 vit D3 can bind to DBP and go into the bone, to increase breakdown, the gut, to increase calcium absorption, or stay in the kidney to increase calcium resorption
100
Q

What is the active form of vit D?

A

1,25-OH2 D3 also known as calcitriol

101
Q

How does calcium play a role in the production of calcitriol?

A

high gradient of blood to intracellular Ca2+ is essential, low blood Ca2+ is sensed by parathyroid gland which releases PTH

102
Q

What does calcitriol activate?

A

calcitriol is sent out into the body to activate intracellular signalling pathways

103
Q

How does calcitriol activate genomically (steps)?

A
  1. calcitriol enters the nucleus and binds to VDR
  2. C+VDR binds to the promoter region of mRNA and synthesizes proteins which are pre-calcium binding proteins
  3. the pre-calcium binding proteins undergo post translational modification and are activated by vitK dependent PTM (gamma carboxylation) to turn them into calcium binding proteins
104
Q

VDR

A

vitD receptor

105
Q

What is VDR

A

type II steroid hormone receptor, it is a TF that promotes calcium-binding protein synthesis

106
Q

How does calcitriol activate non-genomically steps?

A
  1. calcitriol enters the cell via a cell-surface receptor (MARRS) and undergoes protein phosphorylation once inside the cytosol
  2. this causes numerous signally events for example the activation of Ca transporters (Ca2+ can enter the cell)
107
Q

MARRS

A

membrane associated rapid response steroid binding protein
- cell surface receptor

108
Q

What are the three organs relevant for VitD/Ca2+?

A

small intestine
kidney
bone

109
Q

What is the small intestines role in vitD/Ca2+ story?

A

Absorption
- minerals need transporters for absorption by intestinal cells and entry into portal circulation
- proper absorption of Ca2+ depends on the expression of Ca2+ binding proteins in enterocytes

110
Q

What is the kidneys role in vitD/Ca2+ story?

A

Reabsorption
- small molecules like Ca2+ circulate in blood and eventually reach kidney
- pass through filter and can end up in urine unless they are reabsorbed
- reabsorption removes the molecules from the filtrate and gets them back into blood

111
Q

What is bones role in VitD/Ca2+ story?

A

Resorption
- dissolving bone structure to release Ca2+ into the blood
- balance between break down and synthesis allows for bone maintenance, remodeling and repair

112
Q

Difference between osteoclasts and osteoblasts?

A

osteoclasts resorb bone
osteoblasts build bone

113
Q

What is more important, maintaining blood Ca2+ or Ca2+ reserves?

A

maintaining blood Ca2+ is more important than maintaining Ca2+ reserves in bone

114
Q

What is PTH’s role in blood Ca?

A

serves to increase blood Ca
- promotes the production of calcitriol in kidney by activating 1-hydroxylase enzyme
- stimulates bone resorption by activating osteoclasts
- maximizes tubular reabsorption of calcium into the kidney

115
Q

What is vitamin D (calcitriol) role in blood Ca

A

serves to increase blood Ca
- stimulates Ca2+ resorption from bone
- helps to increase absorption of Ca2+ from intestine
- maximizes tubular reabsorption of Ca2+ in kidney

116
Q

What is calcitonin’s role in blood Ca?

A

serves to decrease blood Ca2+
- suppresses tubular reabsorption of Ca2+ in kidney
- inhibits bone resorption and facilitates remineralization

117
Q

Where is calcitonin secreted from?

A

secreted by parafollicular cells in the thyroid

118
Q

Does vitamin D deficiency vary across lifespan?

A

yes

119
Q

What is the composition of normal bone?

A

mixture of solid (outer) and spongy (inner) parts
solid part is 60% mineral (Ca2+ and P) and 40% organic (collagen)

120
Q

What happens with vitamin D deficiency in infants?

A

Rickets (poor mineralization)

121
Q

What is rickets?

A

bones don’t mineralize properly and can’t support the body’s weight when they start walking (permanent and reversible only with surgery)

122
Q

What happens with vit D deficiency in adolescents to adult?

A

osteomalacia

123
Q

What is osteomalacia?

A

bones become demineralized (can be reversed with supplementation), bone fractures can occur more easily, will get worse with time if not corrected

124
Q

What happens with vit D deficiency in middle-aged to eldery?

A

osteoporosis

125
Q

What is osteoporosis?

A

normal part of aging (loss of both mineral and organic parts of bone), diagnosed with bone density scans, difficult to reverse due to erosion of bone (holes in bone form), can take vit D supplements to manage

126
Q

What is osteoporosis worsened by?

A

chronic low Ca2+ vit D and or vit K intake

127
Q

What is the difference between men and women for osteoporosis?

A

men have higher peak bone mass between 20-30 years and lower bone loss

128
Q

What is a big change of the RDA’s of vit D?

A

in recent years, Health Canada tripled the RDA for Vit D

129
Q

How are there not toxicity concerns for vitamin D production from sun exposure?

A

production of Vit D3 is limited by finite amounts of 7-D present in the skin, also produces the inactive lumisterol and tachysterol metabolites with prolonged sun exposure, which have no bioactivity

130
Q

What happens with very high dietary intake of vit D causing high levels of circulating calcitriol?

A

hypercalcemia, leading to a possible calcification of soft tissues, and acute kidney injury

131
Q

Is vitD toxicity rare?

A

yes however it could happen if a person consumes lots of fortified foods, takes dietary supplements and spend lots of time in the sun

132
Q

What is vit K important for?

A

bone formation and blood coagulation

133
Q

How is vit K obtained?

A

through consumption of green leafy plants (as phylloquinone)
made by gut bacteria (as menaquinone)

134
Q

What is a special feature of phylloquinone?

A

sensitive to light and heat

135
Q

Why do infants have poor vit K status?

A
  • little vit K in mothers milk and babies aren’t getting leafy plants yet
  • babies also haven’t developed their colonic gut bacteria so no menaquinone
  • babies given vit K heel prick at birth
136
Q

Is vit K deficiency rare in adults?

A

yes, due to bacterial production

137
Q

Does phylloquinone require digestion?

A

no

138
Q

How is phylloquinone absorbed?

A

incorporated into micelles and absorbed in the small intestine
absorbed via NPC1L1 transporter

139
Q

How are menaquinones absorbed?

A

passive absorption, don’t require a transporter, go into lymphatic system

140
Q

How do phylloquinone and menaquinone transported to various tissues across the body?

A

both are incorporated into chylomicrons

141
Q

Where can vit K be stored?

A

lungs, kidneys, adrenal glands, bone

142
Q

What is the difference between phylloquinone and menaquinone in structure?

A

phylloquinone has a long s.c. and menaquinone doesn’t

143
Q

What are the short forms for phylloquinone and menaquinone

A

phylloquinone - K1
menaquinone - K2

144
Q

What are the steps to the vitamin K cycle?

A
  1. vit K (quinone) comes in from dietary intake or from bacteria
  2. vit K (quinone) ——> vitamin K hydroquinone (active form)
    enzyme: quinone reductase
    NADPH -> NADP+
  3. vitamin K hydroquinone (active) —> vitamin K epoxide (inactive)
    enzyme: gamma-glutamyl carboxylase
    glutamic acid in
    gamma carboxyglutamic acid out
    CO2 in
  4. vitamin K epoxide (inactive) —> vitamin K quinone
    enzyme: epoxide reductase
    warfarin inhibits epoxide reductase
145
Q

What does warfarin do?

A

inhibits epoxide reductase
- rat poison
- anticoagulant

146
Q

What is the reduced form of vit K

A

vit K hydroquinone

147
Q

What is the oxidized form of vit K

A

vit K epoxide

148
Q

how do protein precursors become calcium-binding proteins through the help of vit K steps?

A
  1. protein precursor with a glutamate s.c. becomes a posttranslationally modified protein with a gamma carboxyglutamate s.c. through the gamma-glutamyl carboxylase
  2. posttranslationally modified protein becomes a calcium-binding protein
    - Gla residues on blood clotting proteins bind Ca2+
149
Q

What do Gla residues on blood clotting proteins do?

A

Bind Ca2+. Ca2+ allows gla containing proteins to bind to phospholipids on membrane of blood platelets and endothelial cells

150
Q

What are the susceptible populations for a vit K deficiency?

A

newborn infants
people who take antibiotics regularly
- antibiotics destroy the gut bacterial community
people with malabsorptive illnesses

151
Q

What are deficiency symptoms related to role in gamma-carboxylation in vit K deficiency?

A

impaired blood clotting: possible hemorrhagic syndrome (mostly seen in newborns)
impaired activation of calcium-binding proteins: accelerate development of osteoporosis (mostly seen in elderly adults)

152
Q

What part of the body has the most calcium?

A

bones and teeth

153
Q

Where is calcium primarily obtained?

A

dairy products, but also high in sardines, salmon and some green leafy vegetables, present in these foods as an insoluble salt, stomach acid creates soluble Ca2+

154
Q

Where is calcium absorbed?

A

small intestine, about 25-30% of dietary calcium is absorbed

155
Q

How is calcium absorbed?

A
  • saturable, carrier-mediated, active transport
  • absorption is regulated by calcitriol, most calcium is absorbed this way
  • diffusion via paracellular route is a secondary pathway for Ca2+ uptake
156
Q

What are the ways calcium is transported across the body?

A

40% bound to albumin
10% found complexed with sulfate, phosphate etc.
50% found in free (ionized) form

157
Q

What is the function of calcium?

A

Bone: makes up hydroxyapatite which is what gives strength and rigidity to the bone
Intra- and extracellular calcium (ionized calcium):
- blood clotting (formation of gla residues on coagulation proteins)
- skeletal muscle contraction (release of calcium stores)
- nerve potential (acting through ion channels)
- intracellular signalling pathways

158
Q

What happens to calcium is intra- and extracellular levels drop?

A

bone will be sacrificed

159
Q

How is calcium absorbed from the small intestine to the blood steps?

A
  1. free Ca2+ enters two ways
    - TRPV5/6 transporter (transcellular)
    - through space between cells (paracellular)
  2. transcellular
    - high Ca2+ on lumen side and low Ca2+ on inside of cell
    - the transporter under the influence of proteins made by calcitriol brings Ca2+ into the cell
    - calbindin-D binds to Ca2+ and throws it into the blood through various Ca channels
    • one requires ATP, the other uses
      Na+ gradient
  3. paracellular
    - minor route
    - just a leaking between cells
160
Q

apical vs basolateral

A

the apical surface of the cell faces towards the external environment whereas the basolateral surface sits adjacent to an internal-facing basement membrane.

161
Q

How has the UL of Ca2+ changed?

A

increased UL in children
decreased UL in adults
decreased UL in >70yrs to prevent kidney stones

162
Q

What are factors that affect calcium absorption?

A
  • caffeine decreases absorption
  • some fibres decrease absorption
  • magnesium and zinc decrease absorption
  • PTH (Vit D) increase absorption
  • pregnancy and lactation increase absorption
163
Q

What does Ca2+ deficiency affect?

A

Bone:
- inadequate mineralization in bone
- rickets in children
- osteomalacia

Muscle:
- tetany: a condition characterized by involuntary muscle contractions

  • evidence for association with hypertension
  • evidence for association with colon cancer
164
Q

What happens when there is a Ca2+ toxicity?

A
  • constipation, bloating and/or gas
  • hypercalcemia (kidney stones)
165
Q

In which food is phosphorus found?

A

widely distributed in food
- found in animal products as phosphorus
- grains as phytic acid

166
Q

Is phosphorus deficiency and toxicity common?

A

widely distributed in food, so deficiency and toxicity are rare

167
Q

Where is phosphorus absorbed?

A

most is absorbed in the small intestine in its ionic form PO43-

168
Q

How is phosphorus absorbed?

A

through passive diffusion (primaru
saturable, carrier-mediated, active transport (NaPi cotransporter) - bind phosphate

169
Q

How is phosphorus transported to various tissue?

A

primarily transported in the blood as organic phosphate (incorporated into phospholipids)

170
Q

Where is phosphorus primarily found in the body?

A

bone but also in molecules key for metabolism (ATP, DNA, RNA, cAMP - through phosphorylation)

171
Q

What does phosphorus play a key role in?

A

phosphorylation

172
Q

Is fluoride found in abundance in the body?

A

no, it is found in trace amounts, not essential

173
Q

How is fluoride absorbed?

A

through passive diffusion (nearly 100% efficiency)

174
Q

How is fluoride transported through the body?

A

as ionic fluoride or bound to plasma proteins

175
Q

What is the major function of fluoride?

A

effects on mineralization of teeth and bones, increases resistance of enamel to acid demineralization by forming fluorapatite (protective layer)

176
Q

What happens during a fluoride deficiency?

A

increased incidence of tooth decay

177
Q

What happens during a fluoride toxicity?

A
  • fluorosis (mottling of the teeth) - cosmetic

NUTR 3210 (17 decks)

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