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
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
3
Q
What is Group III?
A
Micronutrients that act as enzyme cofactors
thiamin, niacin, riboflavin, Vit B6, folate, Vit B12, Biotin, Pantothenic acid
4
Q
What is Group IV?
A
Iron, Copper, and zinc-related divalent cations
5
Q
What does bioactive mean?
A
they can interact with eachother and cause an output, a functional form
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
7
Q
What is iodine used to make?
A
T3 hormone, which regulates synthesis of proteins that control a persons basal metabolic rate
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
9
Q
What is Vit D used to make?
A
Vit D precursors are converted to calcitriol, which regulates calcium levels in the body
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
11
Q
What are the two types of steroid hormone receptors?
A
Type 1 and Type 2
12
Q
What is a Type 1 steroid hormone receptor?
A
- cytosolic
- respond to steroid hormones like estrogen, testosterone, progesterone, glucocorticoids, and mineralcorticoids
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
14
Q
Is iodine high in most foods?
A
No, iodine content of most foods is low
15
Q
Is iodine organic or inorganic
A
inorganic
16
Q
Is iodine water soluble?
A
iodine is highly water soluble
17
Q
Where is iodine found in higher concentrations?
A
in coastal populations compared to mountainous regions, seafood has high concentrations, especially sea greens
18
Q
What is fortification?
A
to increase the nutritional value of food by adding vitamins or minerals
19
Q
How is iodine consumed in north america?
A
through salt fortified with potassium iodine
20
Q
How can iodine be found in the body?
A
dietary iodine can be bound to AA or found free
21
Q
What is iodine converted to?
A
in GI tract, iodine (I) is rapidly converted to iodine (I-) and absorbed
22
Q
Where is iodine absorbed?
A
in the stomach, a bit in the small intestine
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)
24
Q
How much of our bodies iodine is found in the thyroid gland?
A
70-80%
25
What is uptake of I- in the thyroid gland mediated by?
active transport system known as the Na+/I- symporter
26
NIS
Na+/I- symporter
27
Do tissues rely on iodine itself?
no, tissues actually rely on the thyroid hormones made by iodine, T3 and T4
28
What is the process of making T3 and T4 from iodide?
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
4. 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
5. The T3 made in the thyroid is directly used for function in the body
6. the hypothalamus sense low T3 and sends neural signals to the pituitary to cause the release of TSH
7. TSH travels to the thyroid to stimulate the production of more T3
29
What is the function of the T3 hormone?
regulates metabolic rate and growth in many tissues through interaction with the thyroid hormone receptor
30
Is T3's half-life longer than T4?
T3 half-life
31
What does T3 interact with?
Thyroid hormone receptor (THR)
32
THR
thyroid hormone receptor
33
What hormone regulates T3 and T4 production?
TSH
34
How much T3 vs T4 is there in the blood?
50 x more T4 in the blood than T3, but T3 is 100 x more potent
35
THG?
thyroglobulin protein
36
Where is THG produced?
in the thyroid cell (nucleus) and then released in the colloid (lumen), THG is a tyrosine rich protein, it is exocytosed into the colloid
37
What does T4 and T3 stand for?
T4 - thyroxine
T3 - Triiodithyronine
38
What is the function of thyroid hormones?
influence how your body stores and uses energy (effects metabolism)
39
What are the 9 things thyroid hormones control?
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
40
What are some characteristics of the T3 and T4 hormones?
- T3 and T4 are lipophilic (can easily cross plasma membranes)
- T4 is converted into T3 in various tissues (primarily in the liver)
41
What does T3 bind to?
in tissues, T3 binds to THR, which then binds to response elements in the promoter regions of DNA to activates gene expression (mRNA)
42
When T3 indirectly activates gene expression, what do the induced genes effect?
- ATPases (pump Na+ and Ca2+ out of cells) which increases metabolic rate
(Na+ muscle contraction, neuron firing) (Ca2+ signalling events)
- growth hormone (anabolic effects)
43
What happens when there is an iodine deficiency?
- 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)
44
What are the health effects of iodine deficiency?
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
45
What is vitamin A referring to?
a group of compounds known as retinoids
46
What are major forms of vitamin A in the body?
retinol, retinal, retinoic acid and retinyl ester
47
What are carotenes?
precursors for vitamin A, they are a type of carotenoid, which are pigments produced in plants
48
What are animal livers rich in?
retinol and retinyl ester
49
What are orange and dark green vegetables rich in?
beta-carotene
50
What is a retinyl ester composed of?
retinol and FA
51
What do retinyl esterases do?
cleave the FA from the retinol
52
How is vitamin A digested and absorbed steps?
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
53
RBP
retinol binding protein
54
What is taken into circulation when vit A is low?
retinol-RBP
55
What is used to check if there is a vitamin A deficiency?
retinol-RBP
56
What do low levels of retinol-RBP stimulate?
hepatic retinyl esterase
57
What is the ability of vitamin A and beta carotene to pass through membranes?
vitamin A and beta carotene are lipophillic, therefore they are handled like other lipids
58
What are the two fates of beta carotene in the liver?
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
59
Where are retinyl esters stored?
in hepatic stellate cells until needed
60
What happens when retinyl esters are needed?
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
61
RA
retinoic acid
62
What does retinol-RBP do?
brings retinol to cells, and can then be converted into RA
63
What is the function of RA?
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
64
RAR
retinoic acid receptor
65
RXR
retinoid X receptor
66
NHR
nuclear hormone receptor
67
Where are stem cells located?
rapidly dividing stem cells are in all epithelial tissues
68
What happens when there is a vitamin A deficiency in epithelial differentiation steps?
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
69
What is an issue with stem cells and vitamin a deficiency?
keratin is a major problem in all epithelial cells whose expression is regulated by retinoic acid
70
What does vit A deficiency in stem cells cause in various parts of the body?
cornea: xeropthalmia
lungs: respiratory infections
GI tract: diarrhea
skin: folliculosis
71
What are the 5 consequences of vitamin A deficiency?
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
RAE
retinol activity equivalents
73
What is RAE?
RAE accounts for differences in the biological activity of various carotenoids
74
Why is there no UL for beta carotene?
carotenoids prevent deficiency but don't cause toxicity, will just be stored if there are enough
75
What occurs during vitamin A dietary toxicity?
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
What can excessive intake of beta carotene cause?
hypercarotenosis (skin turns yellow-orange)
77
What does the bioactive form of vit D act as?
a hormone, works with other hormones such as parathyroid and calcitonin
78
Where is the bioactive form of vit D made?
liver only
79
What are the five forms of vitamin D sources
1. natural plant sources (provitamin D2)
2. natural animal sources (provitamin D3)
3. sunlight
4. supplementation
5. fortification
80
What is an example of a natural plant source that provides vitamin D
shitake mushrooms
81
What is an example of a natural animal source that provides vitamin D
fish, fish liver oils
82
Is vitamin D very active in plants?
no, so plant sources are not a very good source of vitamin D
83
Which provitamin D2 is more bioactive?
(D3) cholecalciferol is more bioactive than (D2) ergocalciferol
84
How is vitamin D made in the skin?
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
How does vitamin D3 circulate around the body?
D3 binds to the vit D binding protein (DBP) and circulates throughout the body
86
How does melanin slow down vit D3 production?
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
What bioactive form of vitamin D is used in supplements?
Vit D3
88
Where is fortification of vitamin d found?
milk and margarine, insufficient for health if this is a persons only source of vit D3
89
Is there a risk of vitamin D toxicity from the sun?
no
90
What are the steps to vitamin D3 production in the skin?
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
What are the steps to vitamin D3 production in the diet?
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
Is there a difference between sun derived vitamin D3 and diet-derived vitamin D3?
no
93
What is vitamin D3 converted to in the liver?
Vit D3 ->(25-hydroxylase) 25-OH
94
What are the steps to vitamin D3 conversion in the liver?
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
what type of enzyme is 25-hydroxylase?
a cytochrome p450 enzyme
96
What is a sign of vitamin D3 deficiency?
if 25-OH D3 levels in the blood are low
97
What happens with regards to vitamin D when calcium levels are low in the body?
25-OH D3 will be converted to an active molecule
98
Does vitamin D regulate calcium homeostasis?
yes
99
What are the steps to forming the active form of vitamin D3 after D3 is converted to 25-Oh D3 in the liver?
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
What is the active form of vit D?
1,25-OH2 D3 also known as calcitriol
101
How does calcium play a role in the production of calcitriol?
high gradient of blood to intracellular Ca2+ is essential, low blood Ca2+ is sensed by parathyroid gland which releases PTH
102
What does calcitriol activate?
calcitriol is sent out into the body to activate intracellular signalling pathways
103
How does calcitriol activate genomically (steps)?
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
VDR
vitD receptor
105
What is VDR
type II steroid hormone receptor, it is a TF that promotes calcium-binding protein synthesis
106
How does calcitriol activate non-genomically steps?
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
MARRS
membrane associated rapid response steroid binding protein
- cell surface receptor
108
What are the three organs relevant for VitD/Ca2+?
small intestine
kidney
bone
109
What is the small intestines role in vitD/Ca2+ story?
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
What is the kidneys role in vitD/Ca2+ story?
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
What is bones role in VitD/Ca2+ story?
Resorption
- dissolving bone structure to release Ca2+ into the blood
- balance between break down and synthesis allows for bone maintenance, remodeling and repair
112
Difference between osteoclasts and osteoblasts?
osteoclasts resorb bone
osteoblasts build bone
113
What is more important, maintaining blood Ca2+ or Ca2+ reserves?
maintaining blood Ca2+ is more important than maintaining Ca2+ reserves in bone
114
What is PTH's role in blood Ca?
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
What is vitamin D (calcitriol) role in blood Ca
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
What is calcitonin's role in blood Ca?
serves to decrease blood Ca2+
- suppresses tubular reabsorption of Ca2+ in kidney
- inhibits bone resorption and facilitates remineralization
117
Where is calcitonin secreted from?
secreted by parafollicular cells in the thyroid
118
Does vitamin D deficiency vary across lifespan?
yes
119
What is the composition of normal bone?
mixture of solid (outer) and spongy (inner) parts
solid part is 60% mineral (Ca2+ and P) and 40% organic (collagen)
120
What happens with vitamin D deficiency in infants?
Rickets (poor mineralization)
121
What is rickets?
bones don't mineralize properly and can't support the body's weight when they start walking (permanent and reversible only with surgery)
122
What happens with vit D deficiency in adolescents to adult?
osteomalacia
123
What is osteomalacia?
bones become demineralized (can be reversed with supplementation), bone fractures can occur more easily, will get worse with time if not corrected
124
What happens with vit D deficiency in middle-aged to eldery?
osteoporosis
125
What is osteoporosis?
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
What is osteoporosis worsened by?
chronic low Ca2+ vit D and or vit K intake
127
What is the difference between men and women for osteoporosis?
men have higher peak bone mass between 20-30 years and lower bone loss
128
What is a big change of the RDA's of vit D?
in recent years, Health Canada tripled the RDA for Vit D
129
How are there not toxicity concerns for vitamin D production from sun exposure?
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
What happens with very high dietary intake of vit D causing high levels of circulating calcitriol?
hypercalcemia, leading to a possible calcification of soft tissues, and acute kidney injury
131
Is vitD toxicity rare?
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
What is vit K important for?
bone formation and blood coagulation
133
How is vit K obtained?
through consumption of green leafy plants (as phylloquinone)
made by gut bacteria (as menaquinone)
134
What is a special feature of phylloquinone?
sensitive to light and heat
135
Why do infants have poor vit K status?
- 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
Is vit K deficiency rare in adults?
yes, due to bacterial production
137
Does phylloquinone require digestion?
no
138
How is phylloquinone absorbed?
incorporated into micelles and absorbed in the small intestine
absorbed via NPC1L1 transporter
139
How are menaquinones absorbed?
passive absorption, don't require a transporter, go into lymphatic system
140
How do phylloquinone and menaquinone transported to various tissues across the body?
both are incorporated into chylomicrons
141
Where can vit K be stored?
lungs, kidneys, adrenal glands, bone
142
What is the difference between phylloquinone and menaquinone in structure?
phylloquinone has a long s.c. and menaquinone doesn't
143
What are the short forms for phylloquinone and menaquinone
phylloquinone - K1
menaquinone - K2
144
What are the steps to the vitamin K cycle?
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
What does warfarin do?
inhibits epoxide reductase
- rat poison
- anticoagulant
146
What is the reduced form of vit K
vit K hydroquinone
147
What is the oxidized form of vit K
vit K epoxide
148
how do protein precursors become calcium-binding proteins through the help of vit K steps?
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
What do Gla residues on blood clotting proteins do?
Bind Ca2+. Ca2+ allows gla containing proteins to bind to phospholipids on membrane of blood platelets and endothelial cells
150
What are the susceptible populations for a vit K deficiency?
newborn infants
people who take antibiotics regularly
- antibiotics destroy the gut bacterial community
people with malabsorptive illnesses
151
What are deficiency symptoms related to role in gamma-carboxylation in vit K deficiency?
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
What part of the body has the most calcium?
bones and teeth
153
Where is calcium primarily obtained?
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
Where is calcium absorbed?
small intestine, about 25-30% of dietary calcium is absorbed
155
How is calcium absorbed?
- 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
What are the ways calcium is transported across the body?
40% bound to albumin
10% found complexed with sulfate, phosphate etc.
50% found in free (ionized) form
157
What is the function of calcium?
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
What happens to calcium is intra- and extracellular levels drop?
bone will be sacrificed
159
How is calcium absorbed from the small intestine to the blood steps?
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
apical vs basolateral
the apical surface of the cell faces towards the external environment whereas the basolateral surface sits adjacent to an internal-facing basement membrane.
161
How has the UL of Ca2+ changed?
increased UL in children
decreased UL in adults
decreased UL in >70yrs to prevent kidney stones
162
What are factors that affect calcium absorption?
- caffeine decreases absorption
- some fibres decrease absorption
- magnesium and zinc decrease absorption
- PTH (Vit D) increase absorption
- pregnancy and lactation increase absorption
163
What does Ca2+ deficiency affect?
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
What happens when there is a Ca2+ toxicity?
- constipation, bloating and/or gas
- hypercalcemia (kidney stones)
165
In which food is phosphorus found?
widely distributed in food
- found in animal products as phosphorus
- grains as phytic acid
166
Is phosphorus deficiency and toxicity common?
widely distributed in food, so deficiency and toxicity are rare
167
Where is phosphorus absorbed?
most is absorbed in the small intestine in its ionic form PO43-
168
How is phosphorus absorbed?
through passive diffusion (primaru
saturable, carrier-mediated, active transport (NaPi cotransporter) - bind phosphate
169
How is phosphorus transported to various tissue?
primarily transported in the blood as organic phosphate (incorporated into phospholipids)
170
Where is phosphorus primarily found in the body?
bone but also in molecules key for metabolism (ATP, DNA, RNA, cAMP - through phosphorylation)
171
What does phosphorus play a key role in?
phosphorylation
172
Is fluoride found in abundance in the body?
no, it is found in trace amounts, not essential
173
How is fluoride absorbed?
through passive diffusion (nearly 100% efficiency)
174
How is fluoride transported through the body?
as ionic fluoride or bound to plasma proteins
175
What is the major function of fluoride?
effects on mineralization of teeth and bones, increases resistance of enamel to acid demineralization by forming fluorapatite (protective layer)
176
What happens during a fluoride deficiency?
increased incidence of tooth decay
177
What happens during a fluoride toxicity?
- fluorosis (mottling of the teeth) - cosmetic
