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Lecture 1

NUTR 3210 Lecture 1: Vitamins and Minerals (P1)

16 Pages
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Department
Nutrition
Course Code
NUTR 3210
Professor
Monk

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Vitamins and Minerals: Part 1
Iodine/Iodide
The mineral iodine exists as I2 (elemental iodine) or as the anion iodide (I-),
iodide is the form we find in our diet
A lot of geographical areas are deficient in iodine, with close to 30% of the
worlds population estimated to live in areas of deficiency; rain washes iodide
out of most inland soils
Iodide is very water soluble, so it is found concentrated in the ocean,
consequently, seafood is a good dietary source, and intake is higher in coastal
populations
People in many countries, even in geographical deficient areas, are exposed to
adequate iodine in the diet b/c of iodide fortification of salt; however, even
some developed countries are surprisingly devoid of fortification programs
Iodine & Thyroid Hormones
The only role of iodide in the body is to participate in the synthesis of thyroid
hormones
Thyroid hormones include T3 (triiodothyronine) and T4 (thyroxin)
T3 is the bioactive form of the hormone and can be made from T4;
T is atuall osidered the prohoroe, or preursor horoe to T
With good iodide status, the ratio of T4:T3 in the blood is 20:1 and the T4
pools acts as a reserve for T3 formation
T3 binds to a steroid hormone receptor called thyroid hormone receptor (THR)
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2
Iodide Digestion, Absorption & Digestion
Dietary iodide will be well absorbed across the small instestine and to the blood it travels by
active transport through to the thyroid gland
T3/THR complex will function as a transcription factor and influence gene expression
How does Iodide Make Thyroid Hormones?**
Once in the thyroid, iodide reacts with hydrogen peroxide to forma radical (I-), a reactive iodide
species
It attacks to the tyrosine ring, and iodinized thyroglobulins cross link together
Enzymes then cleave to cross linked protein to release the smaller thyroid hormone molecules
Both T4 and T3 can be made this way, although the vast majority of T3 is formed from T4 in the
liver
this ia very unique situation, in which there is a chemical production of a hormone that
takes plae o the surfae of a protei, as a post-traslatioal odifiatio
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Thyroid Hormone Signaling
1. T3 is lipophilic and crosses the plasma membrane
- In the nucleus it binds to THR and forms a T3/THR complex and acts as a transcription factor to
increase gene expression
- Free THR decreases transcription of downstream genes
2. T3/THR binds to the promoter region of specific regions
3. Gene regulated by T3 signaling (ie gene expression is enhanced by high blood T3 levels)
- Growth hormone synthesis
- Na+-ATPase and Ca2+ ATPase (maintain ionic gradient for cell signaling)
Health Consequences
If dietary and blood iodide are too low, the thyroid is still unable to produce
sufficient T3 and T4
- The pituitary gland further increases blood TSH levels
Excessive stimulation of the thyroid gland results in hyperplasia (new cells)
and hypertrophy (bigger cells), causing the thyroid to enlarge this is called
goiter
Mild goiters can be reversed, but long term it may result in fibrosis and
utltimately cancer, with a poor prognosis for survival
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Description
Vitamins and Minerals: Part 1 Iodine/Iodide • The mineral iodine exists as I2 (elemental iodine) or as the anion iodide (I-), iodide is the form we find in our diet • A lot of geographical areas are deficient in iodine, with close to 30% of the worlds population estimated to live in areas of deficiency; rain washes iodide out of most inland soils • Iodide is very water soluble, so it is found concentrated in the ocean, consequently, seafood is a good dietary source, and intake is higher in coastal populations • People in many countries, even in geographical deficient areas, are exposed to adequate iodine in the diet b/c of iodide fortification of salt; however, even some developed countries are surprisingly devoid of fortification programs Iodine & Thyroid Hormones • The only role of iodide in the body is to participate in the synthesis of thyroid hormones • Thyroid hormones include T3 (triiodothyronine) and T4 (thyroxin) • T3 is the bioactive form of the hormone and can be made from T4; • T4 is actually considered the “prohormone”, or “precursor hormone” to T3 • With good iodide status, the ratio of T4:T3 in the blood is 20:1 and the T4 pools acts as a reserve for T3 formation • T3 binds to a steroid hormone receptor called thyroid hormone receptor (THR) Iodide Digestion, Absorption & Digestion • Dietary iodide will be well absorbed across the small instestine and to the blood it travels by active transport through to the thyroid gland • T3/THR complex will function as a transcription factor and influence gene expression How does Iodide Make Thyroid Hormones?** • Once in the thyroid, iodide reacts with hydrogen peroxide to forma radical (I-), a reactive iodide species • It attacks to the tyrosine ring, and iodinized thyroglobulins cross link together • Enzymes then cleave to cross linked protein to release the smaller thyroid hormone molecules • Both T4 and T3 can be made this way, although the vast majority of T3 is formed from T4 in the liver  this ia very unique situation, in which there is a chemical production of a hormone that takes place on the surface of a protein, as a “post-translational modification” 2 Thyroid Hormone Signaling 1. T3 is lipophilic and crosses the plasma membrane - In the nucleus it binds to THR and forms a T3/THR complex and acts as a transcription factor to increase gene expression - Free THR decreases transcription of downstream genes 2. T3/THR binds to the promoter region of specific regions 3. Gene regulated by T3 signaling (ie gene expression is enhanced by high blood T3 levels) - Growth hormone synthesis - Na+-ATPase and Ca2+ ATPase (maintain ionic gradient for cell signaling) Health Consequences • If dietary and blood iodide are too low, the thyroid is still unable to produce sufficient T3 and T4 - The pituitary gland further increases blood TSH levels • Excessive stimulation of the thyroid gland results in hyperplasia (new cells) and hypertrophy (bigger cells), causing the thyroid to enlarge  this is called goiter • Mild goiters can be reversed, but long term it may result in fibrosis and utltimately cancer, with a poor prognosis for survival 3 Health Consequences of Iodine Deficiency during pregnancy-Cognitive Impairment/Cretinism • With maternal iodine deficiency, thyroid hormone decrease in the maternal and fetal blood • Thyroid hormones are required for proper fetal development, so maternal iodide deficiency can result in stunted mental and physical growth • Mild impairment is difficult to diagnose but is thought to high a very high world wide prevalence • Severe impairment is recognized as the condition “cretinism” resulting in an ability to walk or talk and a total dependence on others for care Vitamin A • Fat soluble vitamin • The term Vitamin A refers to a number of molecules, including: -retinol (alcohol form) -retinal (aldehyde form, all trans, or 11-cis structures) -retinyl palmitate (an ester formed when retinol reacts with palmityl CoA) -retinoic acid (carboxylic acid form that binds to type II SHR) -certain carotenoids can be converted into retinol, including beta-carotene, which has the greatest pro-vitamin activity • The carotenoids are considered “provitamin A”, or a precursor to vitamin A • The metabolism of vitamin A is complex, and involves formation of a number of metabolites in different tissues -SHR =steroid hormone receptor 4 Vitamin A Molecular Structures • Hypercarotenemia: can occur with a very high level of beta caroene intake • this results from storage of beta carotene in the subcutaneous adipose tissue, giving on organe tinge to the skin • this condition is harmless and the pigment will be eliminated from the body over time when intake decreases Biological Roles of Vitamin A • night vision -as 11 cis retinal (the only function for this molecule) -in the rod cells of the retina, binds with opsin to form rhodopsin which reacts with light to generate a nerve impulse recognized as a dim purple light • retinoic acid functions as a transcription factor to control gene expression and control -cellular differentiation and cell development -growth of epithelial cells (eg: in the intestine epithelial cells = enterocytes) • other effects (retinoic acid functioning as a transcription factor) -Synthesis of glycoproteins, reproduction, bone metabolism, immune function 5 Vitamin A & Night Vision • retinol circulating in the blood as retinol-RBP is taken up by rod cells (responsible for dim light vision) in the retina as retinol, in the rod cell, retinol is converted into all-trans retinal • all trans retinal is converted to 11-cis retinal by an isomerase enzyme -11 cis retinal combines with the protein opsin to make the pigment rhodopsin, also known as “visual purple • when light hits the cis bond in rhodopsin, the molecule bounces back to the all-trans forms (all trans retinal) and releases the opsin, transmitting a nerve impulse via the optic nerve to the brain that registers vision of dim purple light - all trans retinol must be reisomerized in order for the impulse to transmit again • vitamin A circulates as retinol in the bloodrelease it from the carrier in the blood • 11 cis retinal is in its kinked form and will join with opsin to produce rhodopsin • any type of light will hit the 11 cis retinal, will pop it back into trans form • when you are in a bright lit space, light is continuously breaking apart the rhodopsin molecule, since it takes a few seconds for rhodopsin to form, if you suddenly enter a dark room you will be a temporarily blind- once rhodopsin forms again, you will begin to see- but only a dim purple light 6 Retinoic Acid Signaling • key points that show where names of compounds come from • D3: bound to DBP found circulating in the blood • 1,25-diOH D3-enzyme adds on OH group @ carbon 1 • calcitrol: functions as a transcription factor slower process • binds to the MAARA receptor  response is rapid • have to convert retinol to retinoic acid before it can do something functional Vitamin A deficiency World Map • vitamin A deficiency is a significant global health problem, with between 100 and 140 million children are deficient • an estimated 250,000 to 500,000 vitamin A –deficiency children become blind every year, half of them dying within 2 months of losing their sight • 103 million death/year in vitamin A deficiency people caused by infectious disease causing diarrhea, pneumonia, measles 7 Health Consequences of Vitamin A Deficiency • impaired epithelial cell differentiation -can cause permanent blindness and life threatening infections -vitamin A deficiency causes est:1-3 million deaths each year in response to survivable diseases like pneumonia, diarrhea and measles • impaired growth -especially of long bones, too decay • impaired fertility -decreased sperm formation, fetal reabsorption (early death of embryo) • fetal development defects -birth defects due to loss of control of differentiation -can occur with too little or too much vitamin A Health Consequences of Vitamin A Toxicity • also called hypervitaminosis A • Liver Damage -retinyl palmitate (storage form of vitamin A) is stored in the stellate cells of the liver, and with excess vitamin A intake, MORE retinyl palmitate is stored in the cells, which reach full to capacity -the stellate cells proliferate and start to make extra-cellular matrix/scar tissue to accommodate the storage of retinyl palmitate -this eventually starves the hepatocytes of access to nutrients and oxygen death from liver failure can result -usually caused by excessive consumption of liver, or excessive use of vitamin A supplements • Birth Defects -caused by loss of cell differentiation control -Acutane, an acne drug that consists of 13-cis retinoic acid and is essentially a vitamin A supplement, cause birth defects in woman in the early months of pregnancy Vitamin D • Fat soluble vitamin • Is formed from the precursor 7-dehydrocholesterol following exposure to UV light • Both plans and animals make vit D, which can then be consumed by humans or the huans can synthesize their own vitamin D from sunlight, which provides much higher levels • Humans mainly consume the D3 form (animal form), and that is the form they make endogenously • In the body, D3 is metabolized through 2 hydoxylation reactions to 24-OH vitamin D in the liver (the primary form circulating in the blood) and 1,25-diOH vitamin D in the kidney (the form that binds to the type II SHR) - 1,25-OH form is the form that is used in our body and actually functions (the bioactive form) 8 -both D2 and D3 can be consumed as supplements, but D3 (Calcidiol) 1,25 diOH vitamin D (calitriol) -10-15 mins of noon the sun equivalent to 10,000 IU of dietary D3 -following exposure to sunlight (UV rays and then inra-red/heat), 7-dehydrocholesterol is converted to vitamin D3 in the keratinocytes of the skin -previtamin D3 can convert to lunisterol & t
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