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Kin110_Chapter 7 Vitamins (Fat Soluble).docx

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Department
Biomedical Physio & Kines
Course
BPK 110
Professor
Gina Whitaker
Semester
Summer

Description
Kin110 Chapter 7 Vitamins (Fat Soluble) Vitamin A Vitamin A is found in two forms Retinoids -derived from animal sources -preformed vitamin A (biologically active form) -includes retinal, retinol, and retinoic acid Carotenoids -derived from plant sources (yellow-orange pigments) -pro-vitamin form, converted to retinoid form by body as needed Examples include β-carotene, lycopene, lutein Functions Vision Retinal forms part of the molecule called rhodopsin -rhodopsin is found in the cells of the retina (back of eye) -important for converting a light stimulus to an electrical signal which allows brain to interpret visual info After entering the eye, light strikes the visual pigment rhodopsin, which is formed by combining retinal with the protein pepsin Light causes the retinal molecule to change from a bent to a straight configuration A nerve signal is sent to the brain, telling that there is light, and retinal is released from opsin Some retinal is lost in the cycle Some retinal returns to its original configuration and binds to opsin to being the cycle again When vitamin A status is normal, vitamin A from the blood replaces any retinal lost from the cycle When vitamin A is deficient, not enough vitamin A is available in the blood, and the regeneration of rhodopsin is delayed. Until rhodopsin reformed, light cannot be perceived Cell differentiation (immature stem cells → specialized mature cells) Vitamin A increases/decreases gene expression (the events of protein synthesis in which the information coded in a gene is used to synthesize a protein) E.g. express a specific gene which tells cell to make a specific protein which affects function of a cell Vitamin A promotes differentiation of epithelial cells -skin, lining of eyes, intestines, lungs, vaginal tissue, bladder Vitamin A promotes differentiation of T-lymphocytes -immune function Reproduction & Growth (due to its function in cell differentiation) Retinol important for sperm development Required for normal fetal growth Important for bone remodeling (process by which old bone is removed and new bone is formed) and growth Antioxidant (carotenoids only) Donates an electron to oxygen free radicals to prevent them from stealing electrons from other molecules RDA = 700 ug (women) & 900 ug (men) E.g. 100% RDA-1 cup sweet potatoes, ½ cup pumpkin, or ½ cup carrots Deficiency One of the most common nutrient deficiencies worldwide Leading cause of preventable blindness Deficiency due to lack of intake required 1-2 years to develop in adults (more quickly in children) -can also be due to a lack of fat intake First detectable sign is night blindness (difficulty seeing in dim light which is reversible with additional vitamin A) -early stage of xerophthalmia (spectrum of eye conditions resulting from vitamin A deficiency that may lead to blindness) Increased incidence of infectious disease Keratinization/Hyperkeratosis -epithelial cells don’t differentiate properly and begin to secrete keratin instead of mucus -keratin is a hard inflexible protein (found in hair and finger nails) -later stage xerophthalmia is total blindness due to drying and hardening of the cornea -skin becomes dry, rough and scaly Toxicity Only the retinoid form is toxic Overconsumption of carotenoids is not harmful because conversion to retinoids is regulated in the body however; it may lead to a harmless condition known as hypercarotenemia (a condition caused by the accumulation of carotenoids in the adipose tissue, causing the skin to appear yellow-orange) Symptoms of Toxicity -nausea, vomiting, diarrhea -loss of appetite, fatigue, insomnia -headaches, blurred vision, dizziness -liver damage, bone fractures -abnormal fetal development & birth defects Vitamin A toxicity can be fatal Vitamin D (The sunshine vitamin) Can be obtained from the diet or the sun -diet form is the inactive form -vitamin D precursor made from cholesterol sits beneath the skin and is converted to inactive Vitamin D by UV rays Inactive Vitamin D is modified by both liver and kidneys to become active Activation & Function We get vitamin D from the diet and from synthesis in the skin In order to function, vitamin D must be chemically modified first by the liver and then by the kidneys At the intestine, active vitam
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