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FScN 1112 > Chapter 12 Fat Soluble Vitamins > Flashcards

Chapter 12 Fat Soluble Vitamins Flashcards

(96 cards)

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1
Q

Where can vitamin ADEK dissolve in?

A

Organic solvents such as ether and benzene. They are referred to fat-soluble vitamins.

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2
Q

Where can vitamin B and C dissolve in?

A

Water. They are called water-soluble vitamins.

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3
Q

Why vitamin important in diet?

A

Because it cannot be synthesized in body.

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4
Q

How to qualify a substance as vitamin?

A

Health decline when the substance is not consumed.

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5
Q

Absorption of vitamins

A

Vitamin ADEK are absorbed together with fat. It depends on efficient bile and pancreas use. 40% to 90% of fat soluble vitamin can be absorbed, and 90% to 100% of water-soluble vitamin can be absorbed. It happens in small intestinal.

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6
Q

What can lead to malabsorption of vitamin?

A

Alcohol abuse and certain intestinal disease.

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7
Q

Where will vitamin be transported after absorption?

A

lymphatic system and delivered by the bloodstream to target cells throughout the body in a manner similar to that for dietary fats.

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8
Q

Where are the vitamins stored in the body

A

Except vitamin K, fat-soluble vitamin are not readily to excrete from body. They are stored in the liver and adipose tissue. And water-soluble vitamins are excreted rapidly.

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9
Q

Two vitamins which has greater storage than other water-soluble.

A

Vitamin B12 and B6.

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10
Q

The vitamin toxicity most likely occur?

A

Vitamin A and D.

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11
Q

When will vitamin toxicity occur?

A

Vitamin toxicity is unlikely to occur unless the amount of intake is 5 or 10 times to the DRI.

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12
Q

Retinoid

A

A collective term for the biologically active forms of vitamin A. It is called performed because it does not need to be converted in the body to become biological active.

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13
Q

Three forms of retinoid

A

Retinol(alcohol), retinal(aldehyde), and retinoic acid.

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14
Q

Carotenoid

A

Are yellow-orange pigment material in fruits and vegetables. They can be converted into vitamin A. Only alpha-carotenoid, beta and beta-crypotoxanthin can be converted to vitamin. Thus other carotenoid do not have vitamin A activity in body.

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15
Q

Where can retinoid be found?

A

Liver. fish, fish oil, fortified milk, and eggs.

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16
Q

Where can carotenoid found?

A

Dark green and yellow- orange vegetables and fruits, such as carrots, spinach and other greens.

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17
Q

Beta-carotene

A

It has the greatest amount of provitamin A activity. It provide the yellow-orange color to vegetables and fruits. The color is masked by the green color provided by the chlorophyll. Therefore, consuming a varied amount of dark green food and yellow-orange food can provide VA.

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18
Q

Unit for vitamin A

A

UI in the past. Milligram or microgram now.

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19
Q

How to express vitamin A activity in diet?

A

RAE (Retinal Activity Equivalent).

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20
Q

1 RAE equals to

A

1 microgram retinol, 12 microgram beta-carocarotene, and 24 μg of the other 2 provitamin A carotenoids.

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21
Q

RE

A

Retinol Equivalent. Older measurement for vitamin A activity. 1RE = 1 RAE. Actually food contains less vitamin A than RE and UI suggest.

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22
Q

RDA for vitamin A

A

900 microgram RAE per day for men and 700 for women.

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23
Q

What compounds are performed vitamin A found in food?

A

retinol and retinyl ester compounds. Retinol compounds attached with fatty acid. Retinyl ester doesn’t have vitamin A activity until retinol separate from fatty acid in intestinal acid.

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24
Q

How much retinol can be absorbed ?

A

90% can be absorbed into cells of small intestinal via specific carrier protein.

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25
What happened after absorption
A retinol attached with a fatty acid and form a new retinyl ester compound. These retinyl esters are packaged into chylomicrons before entering the lymphatic circulation.
26
Digestion of carotenoid
Carotenoid is attached with proteins that must be split off before absorption. Once freed, it will be absorbed primarily by passive diffusion.
27
Absorption range of carotenoid
5% to 60% of intake.
28
After vitamin A released from liver
It is bound to a retinol-binding protein.
29
Synthesis of RBP needs
Retinol-binding protein. The synthesis of RBP needs adequate amount of retinol, protein, and zinc.
30
What happened when retinol in the bloodstream?
They are bound with another protein called transthyretin.
31
What happened after carotenoid released from liver?
They are carried by lipoproteins and are taken up into cells by specifi c apoprotein receptors.
32
The distribution of RBPs
Differs among tissues, possibly reflecting their different functional needs for vitamin A.
33
Excretion of vitamin A
Retinoid is excreted via urine. Carotenoid is excreted via bile that is eliminated with feces.
34
Key function of retinoid.
Development and growth, cell differentiation, vision, and immune function.
35
Role of VA during the embryonic
VA is involved in the development of eyes, limbs, the cardiovascular system, and the nervous system.
36
What happens if lack of VA during the pregnancy ?
Birth defects and fetal mortality.
37
The function of retinol acid
Production, structure, and normal function of epithelial cells in the lungs, trachea, skin, and GI tract, as well as in many other systems. It is important for the formation and maintenance of mucous-forming cells in these organs.
38
The function of cell differentiation
In the cell nucleus, retinoid bind to 2 main families of retinoid receptors. These receptors bind with DNA site that regulate the formation of RNA and the subsequent formation of protein through gene expression. Gene expression directs cell-differentiation.
39
Role of rods in eyes
Rods are responsible for the visual processes that occur in dim light, translating objects into black-and-white images and detecting motion.
40
Role of cones
Cones are responsible for the visual processes occurring under bright light, translating objects into color images.
41
VA in eyes
In the rods, 11-cis-retinal binds to a protein called opsin to form the visual pigment rhodopsin. Some is stored in the eye to maintain vitamin A pools. If vitamin A pools become depleted, the process of dark adaptation is impaired, making it diffi cult to adjust to seeing in dim light, known as night blindness.
42
Why VA help immune system
Vitamin A helps maintain the epithelium, a barrier that protects the body against the entry of disease pathogens
43
What disease is VA treated
Dermatology like acne and psoriasis. Also used topically to lessen the damage from excess sun and UV-light exposure.
44
Function of carotenoid
Decrease eye disease, cancers, and cardiovascular diseases.
45
Beta-carotene
Most familiar carotenoid. Beta-carotene may act as an antioxidant within tissues, thereby protecting them from free radical damage.
46
Beta-carotene supplements cannot
reduce the risk of cancer, and may even increase the risk of certain individuals. No direct related to preventing macular degeneration.
47
lycopene
番茄红素
48
lycopene can help to
reduce the risk of CVD. Because they can inhibit oxidation of the lipoprotein. Beta-carotene supplementation alone has not been consistently shown to decrease risk of CVD.
49
Instead of carotenoid supplements
Carotenoid supplements are not recommended, but vegetables and fruits rich of it is advocated.
50
Deficiency of VA
Blind. Keratomalacia(角膜软化)，xerophthalmia(眼球干燥症)，follicular hyperkeratosis(毛囊角化过度)
51
Hypervitaminosis A
Use 5 or 10 time of RDA of VA
52
Upper level for retinol
3000 microgram.
53
Upper level for carotenoid
No upper level, because hypervitaminosis A is not caused by it.
54
Three kinds of VA toxicity
Acute, chronic, and teratogenic
55
Acute VA Toxicity
Caused by ingestion 1 very large dose of VA or several doses. About 100 times.
56
Symptom of acute VA T
GI tract upset, headache, blurred vision, and poor muscle coordination. 500 mg for children and 10 g for adults is fatal.
57
Chronic VA T
10 times of RDA
58
Symptom of chronic VA T
Joint pain, loss of appetite, skin disorders, headache, reduced bone minerals, liver damage, double vision, hemorrhage, and coma.
59
Teratogenic VA T
Most tragic effects. Cause birth defects and spontaneous abortion.
60
Vitamin D
Conditional vitamin, prohormone. Intake of vitamin D is essential to prevent the deficiency diseases rickets and osteomalacia and to provide for cellular needs.
61
Food source for V D2
Fatty fish, cod liver oil, fortified milk, and some fortified breakfast cereals. Milk is 10 microgram of VD per quart.
62
How much VD3 is provided by sun?
80% to 100% vitamin required by body.
63
VD3 requirements for old people.
The production of vitamin D3 in the skin decreases by about 70% when one reaches the age of 70.
64
Formation and transportation of VD3
During exposure to sunlight, 1 ring on the molecule undergoes a chemical transformation, forming the more stable vitamin D3 (cholecalciferol). This change allows vitamin D3 to enter the bloodstream for transport to the liver and kidneys, where it undergoes conversion to its bioactive form.
65
Vitamin D needs
5 μg/day (200 IU/day) for people under age 51, 10 μg/day (400 IU/day) for people between 51 and 70, and 15 μg/day (600 IU/day) for older adults.
66
Absorption of VD
VD comes from food and synthesized in skin. Dietary VD is absorbed in small intestinal. 80% of the VD intake is incorporated into micelles in the small intestine, absorbed and transported to liver through lymphatic system.
67
Calcitriol
The most active form of VD.
68
Functions of calcitriol
Concentrate calcium and phosphorous in body. It release calcium and phosphorus from bones when the blood level low down. Helps regulate immune function and the secretion of several hormones. May decrease the risk of certain types of infections and auto immune diseases.
69
Vitamin D deficiency disease
Rickets. When calcium and phosphorus are released from bone, bones will bent under the pressure.
70
Osteomalacia
vitamin D deficiency for adults. Soft bones.
71
Upper level of VD
50 μg per day. UL of 1000 to 3000 IUs per day for infants and children up to 8 years of age and 4000 IUs per day for individuals 9 years of age and older is more appropriate.
72
VD Toxicity
Excess blood calcium, in turn, leads to deposits of calcium in the kidneys, heart, and lungs; anorexia; nausea; vomiting; bone demineralization; weakness; joint pain; and kidney dysfunction.
73
Why northern people have higher risk of VD deficiency
They have little sun exposure, they also may have reduced vitamin D levels from low dietary intakes and/or impaired kidney function, which limits conversion to the active form of vitamin D.
74
8 naturally occurring compounds
4 tocopherols (alpha, beta, gamma, delta) and 4 tocotrienols (alpha, beta, gamma, delta)
75
Structure of VE
A long carbon chain tail attached to a ringed structure.
76
Food resource for VE
Plant oils, wheat germ, avocado, almonds, peanuts, and sunflower seeds. Products made from plant oils are also good resource, like salad dressings. Animal fats and diary products provide little VE.
77
RDA for VE
15 mg/day for both men and women. The recommended amount of VE is needed to prevent a breakdown of red blood cell membranes.
78
IU convert to mg
1 IU equals 0.45 mg. If VE is natural source, it equals 0.67 mg.
79
How much VE can be absorbed from dietary intake?
Absorption occurs by passive diffusion and can vary from 20 to 70% of dietary intake.
80
Absorption of VE
VE incorporated with micelles in the small intestine, depend on bile and pancreas. vitamin E is incorporated into chylomicrons for transport in the lymph and eventually the blood. As chylomicrons are broken down, most of the vitamin E is carried to the liver as chylo micron remnants. A small amount is carried directly to other tissues. The liver repackages the vitamin E from the chylomicron remnants with other lipoproteins (VLDL, LDL, and HDL) for delivery to body tissues.
81
Function of VE
Maintain the integrity of cell membranes by stopping chain reactions caused by free radicals.
82
VE deficiency
It is rare in humans. People who have greatest risk of deficiency are those with fat malabsorption conditions. (cysticfibrosis or Crohn’s disease, smokers, and preterm infants.) Also impair the immune function and cause neurological changes in the spinal cord and peripheral nervous system.
83
VE toxicity
Excessive VE can interfere with the role of VK in blood clotting. This cause insufficient clotting and risk of hemorrhaging.
84
Family of VK
Phylloquinones (vitamin K1) from plants and menaquinones (vitamin K2)found in fi sh oils and meats.
85
VK sources
10% of VK we absorb is from bacterial synthesis in colon. Rest is from diet. Green leaf vegetables, broccoli, peas, and green beans are best sources. It is heat stable, but can be destroyed under light.
86
VK needs
For women, the Adequate Intake for vitamin K is 90 μg/day; for men, it is 120 μg/day.
87
Absorption of VK
Approximately 80% of dietary vitamin K is taken up by the | small intestine and incorporated into chylomicrons.
88
Function of VK
Vitamin K is needed for the synthesis of blood clotting factors by the liver and the conversion of preprothrombin to the active blood clotting factor called prothrombin. Also plays a role in bone metabolism.
89
VK deficiency
Can occur to newborn infants, because vitamin K stores are typically low at birth and the intestinal tracts of newborns do not yet have bacteria that can synthesize vitamin K.
90
Upper level for VK
No upper level. Injections of menadione can cause anemia.
91
Supplements
Although dietary supplements can replace specific nutrients lacking in a diet, they cannot fully correct a nutritionally poor diet.
92
Women with excessive bleeding during menstruation may need
Iron supplement to prevent anemia.
93
Women who are pregnant or breastfeeding may require
Iron and folate supplements to meet their needs.
94
Individuals with low calorie intakes may require
A multivitamin and mineral supplement to correct for limited intakes.
95
Vegans may require
calcium, iron, zinc, vitamin D, and vitamin B-12 supplements to prevent deficiencies.
96
Newborn
Need VK

FScN 1112 (12 decks)

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