NHM 573 - Exam 3 Study Guide Outline

Which four forms of vitamin E are tocopherols?

Alpha-, beta-, gamma-, and delta-tocopherol.

How do the four tocopherols differ structurally?

They differ in the number and positions of methyl groups on the chromanol ring.

Which tocopherol has the highest biological activity in humans?

Alpha-tocopherol.

How do tocopherols and tocotrienols differ structurally?

Tocopherols have a saturated side chain; tocotrienols have an unsaturated side chain with three double bonds.

What is the main antioxidant function of vitamin E?

It donates hydrogen to lipid peroxyl radicals, stopping membrane lipid-peroxidation chains.

How does vitamin E help protect polyunsaturated fatty acids?

It interrupts free-radical chain reactions that damage PUFAs in membranes and lipoproteins.

How is natural alpha-tocopherol different from synthetic alpha-tocopherol?

Natural vitamin E is typically RRR-alpha-tocopherol; synthetic all-rac-alpha-tocopherol contains eight stereoisomers.

Which form of supplemental vitamin E is often listed as natural?

d-alpha-tocopherol or RRR-alpha-tocopherol.

Which form of supplemental vitamin E is often listed as synthetic?

dl-alpha-tocopherol or all-rac-alpha-tocopherol.

How does vitamin E relate to cardiovascular health through PKC?

Alpha-tocopherol can inhibit protein kinase C activity, affecting cell signaling, vascular smooth-muscle growth, and platelet responses.

How can vitamin E deficiency present?

Neuropathy, ataxia, reduced reflexes, muscle weakness, vision problems, and hemolytic anemia.

Who is at increased risk for vitamin E deficiency?

People with fat malabsorption, pancreatic insufficiency, abetalipoproteinemia, alpha-TTP defects, or prematurity.

What is a major risk of high-dose vitamin E supplementation?

It can impair vitamin K-dependent clotting and increase bleeding risk.

What is the adult UL for supplemental alpha-tocopherol?

1,000 mg/day; high doses can increase bleeding risk.

What are the main forms of vitamin K?

Vitamin K1 is phylloquinone; vitamin K2 includes menaquinones.

What are the main food sources of vitamin K1 and K2?

K1: leafy green vegetables and plant oils. K2: some fermented foods and animal foods.

How are vitamins K1 and K2 transported after intestinal absorption?

They are incorporated into chylomicrons, travel through lymph to blood, and circulate in lipoproteins.

Where is vitamin K stored, and how extensive are its stores?

Stores are limited; some is held in the liver and extrahepatic tissues.

What is vitamin K's role in blood clotting?

It enables gamma-carboxylation of clotting factors II, VII, IX, and X, allowing calcium binding.

Which anticoagulant proteins depend on vitamin K?

Proteins C and S.

How does vitamin K support bone health?

It carboxylates osteocalcin, helping it bind minerals in bone.

How does matrix Gla protein relate to vitamin K?

Vitamin K-dependent carboxylation activates MGP, which helps inhibit vascular calcification.

What is the active form of vitamin K used by gamma-glutamyl carboxylase?

Reduced vitamin K hydroquinone (KH2).

What happens during the vitamin K cycle?

KH2 is oxidized during carboxylation to vitamin K epoxide; enzymes recycle it to the active reduced form.

How does warfarin affect the vitamin K cycle?

It inhibits VKORC1, reducing regeneration of active reduced vitamin K.

Why can warfarin affect blood clotting?

It reduces activation of vitamin K-dependent clotting factors II, VII, IX, and X, as well as proteins C and S.

What is the key difference between preformed vitamin A and provitamin A?

Preformed A comes from animal foods; provitamin A carotenoids come from plants and can be converted to retinoids.

Which carotenoids are provitamin A compounds?

Beta-carotene, alpha-carotene, and beta-cryptoxanthin.

Which carotenoids are not provitamin A?

Lycopene, lutein, and zeaxanthin; they do not convert to vitamin A.

What functions can carotenoids have besides providing vitamin A?

Antioxidant activity; lutein and zeaxanthin also accumulate in the macula and filter some blue light.

What is the RAE conversion for dietary beta-carotene?

12 micrograms of dietary beta-carotene = 1 microgram RAE.

What is the RAE conversion for supplemental beta-carotene?

2 micrograms of supplemental beta-carotene = 1 microgram RAE.

What are the RAE conversions for retinol and other dietary provitamin A carotenoids?

1 microgram retinol = 1 microgram RAE; 24 micrograms dietary alpha-carotene or beta-cryptoxanthin = 1 microgram RAE.

How is vitamin A absorbed from food?

Fat digestion and bile salts support micelle formation; retinoids and carotenoids enter intestinal cells and are packaged into chylomicrons.

What happens to retinyl esters during vitamin A digestion?

Digestive enzymes hydrolyze them to release retinol for absorption.

What happens to retinol inside an intestinal cell?

It binds CRBPII, is re-esterified mainly by LRAT, and is packaged into chylomicrons.

Which enzyme helps convert beta-carotene to retinal?

Beta-carotene oxygenase 1 (BCO1).

What are the functions of retinol, retinal, retinoic acid, and retinyl palmitate?

Retinol: transport/precursor; retinal: vision; retinoic acid: gene regulation; retinyl palmitate: storage ester.

How is vitamin A stored and transported to tissues?

It is stored mainly as retinyl esters in liver stellate cells; retinol travels in blood bound to RBP and transthyretin.

How does retinoic acid regulate gene expression?

It binds RAR; the RAR-RXR complex binds retinoic acid response elements (RAREs) on DNA to regulate transcription.

How does 11-cis-retinal support vision?

It binds opsin to form rhodopsin in rod cells.

What happens when light hits rhodopsin?

11-cis-retinal isomerizes to all-trans-retinal, triggering the visual signaling cascade.

What is the adult UL for preformed vitamin A?

3,000 micrograms RAE/day; it applies to preformed vitamin A, not naturally occurring beta-carotene in foods.

What causes vitamin A deficiency, and what are key signs?

Inadequate intake or absorption can cause night blindness, xerophthalmia, Bitot spots, and corneal damage.

What causes vitamin A toxicity, and what are key risks?

Excess preformed vitamin A, especially from supplements or liver, can damage the liver and bones and cause birth defects during pregnancy.

How is vitamin D synthesized in skin?

UVB converts 7-dehydrocholesterol to previtamin D3, which heat converts to vitamin D3.

How is vitamin D activated in the body?

The liver makes 25-hydroxyvitamin D; the kidney makes active 1,25-dihydroxyvitamin D (calcitriol).

Which blood measure is commonly used to assess vitamin D status?

Serum 25-hydroxyvitamin D [25(OH)D].

How do micrograms of vitamin D convert to IU?

1 microgram vitamin D = 40 IU; 15 micrograms = 600 IU; 20 micrograms = 800 IU.

How does vitamin D regulate calcium homeostasis?

Calcitriol increases intestinal calcium absorption and supports calcium balance through effects on kidney and bone.

What stimulates renal activation of vitamin D?

Low blood calcium stimulates PTH, which increases renal 1-alpha-hydroxylase activity.

Which proteins support active vitamin D-dependent calcium absorption in the intestine?

TRPV6 brings calcium into enterocytes; calbindin-D9k carries it intracellularly; PMCA1b moves it into blood.

How does vitamin D affect immune function?

It supports innate antimicrobial defenses and modulates adaptive immune responses, helping regulate inflammation.

How does calcitriol regulate gene expression?

It binds nuclear VDR; the VDR-RXR complex binds vitamin D response elements (VDREs) to regulate transcription.

What are major signs of vitamin D deficiency?

Rickets in children, osteomalacia in adults, muscle weakness, and impaired bone mineralization.

What are major signs of vitamin D toxicity?

Hypercalcemia, nausea, weakness, confusion, kidney stones, and kidney damage, usually from excessive supplements.