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Biochem Exam 2 > L17 Vitamins > Flashcards

L17 Vitamins Flashcards

1
Q

How was the term vitamin first used?

A

To describe the “vital amine” thiamine: needed to prevent berberi

Berberi was a common disease in people who depended on white rice as their main source of food

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2
Q

What are vitamins?

A

Essential organic molecults that are either not synthesized or inadequately synthesized in the human body

Micronutrients that must be supplied by diet

Some vitamins can be synthesized by human metabolism (Vit D) OR intestinal flora (biotin, Vit K, Vit B12)

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3
Q

How are vitamins named?

A

Letters because chemical structures unknown

Numerical subscripts (B1, B2) for vitamins that were originally thought to be one but turned out to be different

Others were originally designated as different, turned out to be the same compound (Vit H, M, S, W, X are all biotin)

Vit G–>B2 (riboflavin)

Vit Y–>B6 (pyridoxine)

Vit M used for three different vitamins: folic acid, pantothenic acid, biotin

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4
Q

How are vitamins classified?

A

Water v. fat soluble

Non B complex v. B complex

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5
Q

What are the differences in water-soluble vitamins v. fat-soluble vitamins in terms of function?

A

Water-soluble vitamins:

  • most B-complex vitamins acts as a co-enzyme
  • Vit C is an antioxidant

Fat soluble vitamins:

  • Vitamins A: hormone and co-enzyme
  • Vitamin D: hormone
  • Vitamin E: antioxidant
  • Vitamin K: co-enzyme
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6
Q

What is the difference between water-soluble vitamins and fat-soluble vitamins in terms of absorption?

A

Water-soluble:

  • specific membrane transporters

Fat-soluble:

  • Requires bile salts to form mixed micelles and normal CM metabolism
  • Fat malabsorption can cause Vit A, E, K deficiency
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7
Q

What is the difference between water-soluble vitamins and fat-soluble vitamins in terms of storage?

A

Water-soluble:

  • generally not stored in excess quantities
  • exceptions are B6 and B12

Fat-soluble:

  • Liver: Vit A
  • Adipose: Vit D and E
  • Vit K is not stored
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8
Q

What is the difference between water-soluble vitamins and fat-soluble vitamins in terms of urinary excretion?

A

Water-soluble: readily excreted

Fat-soluble: not readily excreted

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9
Q

What is the difference between water-soluble vitamins and fat-soluble vitamins in terms of excess intake?

A

Water-soluble:

  • generally not toxic
  • Upper limits are set for niacin, vit C, B6, and folate

Fat-soluble:

  • toxic or adverse effects if high quantities are ingested except for Vit K
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10
Q

Where are water-soluble vitamins found?

A

Found in fruits and vegetables and animal products

  • Vit B12 (cobalamin): eggs, milk, and milk products, fish
  • Vit C (ascorbic acid): fruits vegetables only

Raw fruits and vegetables should be included in diet: can be destroyed during cooking (eg. Vit C, thiamine, folic acid)

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11
Q

How do vitamin deficiencies manifest?

A

Single vitamin deficiencies are uncommon in the US because most vitamins come from dietary sources

It is more common for people to have multiple deficiences as a result of under-nutrition from food faddism, alcholism, or as a result of other diseases

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12
Q

What leads to vitamin deficiency?

A

A large number of factors

In general, it is determined by the balance between the amount of vitamins that are ingested with the diet, absorbed from the intestine, stored in the body, metabolized, and excreted

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13
Q

How do nutritional factors play a role in vitamin deficiency?

A
  • under nutrtion: food faddism
  • depletion of vitamin source: milling increases shelf life but at the expense of fiber, vitamins, and minerals
  • milling separates the bran (fibrous covering) and germ (plant embryo) leaving starchy less nutritous endosperm
  • wheat flour enriched with four of B vitamins (thiamine, riboflavin, niacin, folic acid) and the mineral iron. enriched products are still low in Vit B6, K+, Mg++ and fiber
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14
Q

What are the factors leading to vitamin deficiency?

A
  • nutritional factors
  • malabsorption due to gastrointestinal diseases or surgery
  • alcoholism
  • reduction of body stores
  • increased demand
  • increased loss
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15
Q

What is enrichment?

A

Replacing nutrients lost is processing or milling

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16
Q

What is fortification?

A

Adding new nutrients that were never present in food previously

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17
Q

How does malabsorption contribute to vitamin deficiency?

A

Crohn disease, cystic fibrosis, fastric resection, bile salt deficiencies

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18
Q

How does alcoholism contribute to vitamin deficiency?

A

Leading cause of multiple vitamin deficiencies in Western countries, including thiamine, niacin, Vit B6, folate, Vit C, A

Multiple mechanisms: Poor diet, malabsorption via interference of transporters, increased demand due to increased carb metabolism from ethanol, and increased exertion

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19
Q

How does alcohol effect thiamine?

A

decreased intestinal absorption

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20
Q

How does alcohol effect riboflavin?

A

decreased intestinal absorption

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21
Q

How does alcohol effect folate?

A

decreased intestinal absorption and decreased renal re-absorption

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22
Q

How does alcohol effect pyridoxal PO4?

A

increased degredation and increased renal excretion

23
Q

How does alcohol effect vitamin A?

A

increased hepatic cytochrome P450–>increased vitamin A degredation

decreased conversion of beta-carotene to vitamin A

24
Q

How does reduction of body stores contribute to vitamin deficiency?

A

Larger body stores, longer it takes to become deficient after depletion

Vit B12 and A have larger body stores which can last for years

Folate and thiamine have short body stores which last for days

25
Q

How does increased demand lead to vitamin deficiency?

A

Demand for vitamins can increase during pregnancy, lactation, alcoholism, and stress (injury, extreme exercise)

26
Q

How does increased loss lead to vitamin deficiency?

A

increased excretion caused by alcoholism or diuretics or hemodialysis (removes water-soluble vitamins)

27
Q

What is hypervitaminosis?

A

Several vitamins have adverse effects if taken in high doses

Upper limits are set. UL is the highest average daily nutrient intake level tha tis likely to pose no risk of adverse health effects to almost all individuals

Vit B6, niacin, folate, Vit C, A, D, and E

28
Q

What is Vitamin A?

What is it good for?

What forms does it exist in?

A

Fat-soluble vitamin

Collective name for retinoid family of molecules required for vision, growth, differentiation, epithelial tissue maintainence, reproduction

Exists as retinol, retinyl phosphate, retinal, and retinoic acid

29
Q

What is retinol and retinal?

A

forms of Vitamin A that are essential for reproduction

30
Q

What is retinyl phosphate?

A

form of vitamin A necessary for synthesis of certain glycoproteins and mucopolysaccharides, which are components of mucus in the eye, GI, and lung

31
Q

What is retinoic acid?

A

form of vitamin A that serves as a hormone

binds to its nuclear receptor and functions as a transcription regulator

similar to the signal transduction mediated by steroid hormones

inhibits the expression of keratin, protein found in hair, nails, skin. this is crucial in corneal tissue in order to keep the cornea crystal clear and unkeratinized

32
Q

What are some issues in early phase of vitamin A deficiency?

What are some facts about vitamin A deficiencies?

A

Night blindness

Hyperkeratosis of skin: dry, rough, scaly

Ethanol increases the levels of liver cytochrome P450 which are responsible for catabolism of vitamin A

Vitamin A deficiency increases mortality associated with infectious disease, but not incidence

Deficiency is US is rare, takes 2 years to deplete liver stores

33
Q

What do you see is severe deficiency of vitamin A?

A

Xerophthalmia: most common cause of blindness worldwide

34
Q

What happens with excess vitamin A?

Where is vitamin A found?

A

Because vitamin A is a hormone, high levels are toxic

Stored in Ito cells of liver

10 x RDA over period of months to years = chronic toxicity

>100 x RDA over period of months to years = acute toxicity

Only animal sources are liver and eggs, milk is fortified with vitamin A, not found in plants

35
Q

What is the principle source of provitamin A in our diet?

A

beta-carotene found in most dark green vegetables, fruits and vegetables that are yellow or red

Ethanol lowers beta-carotene dioxygenase levels and inhibits the conversion of beta-carotene to vitamin A

36
Q

What is vitamin K?

How do we get it?

What is it used for?

A

Fat-soluble vitamin

Vegetables are among the few foods that provide vitamin K

It can also be produced by colonic flora: gut bacteria produce vitamin K2, so deficiency is rare unless adults are taking antibiotics long term

However, unlike other fat-soluble vitamins the body does not store vitamin K, processed in 24-48 hours

Required for carboxylation of glutamate residues in clotting factors (VII, IX, X, II) and bone protein, osteocalcin

Warfarin is a competative inhibitor of vitamin K dependent enzymes

37
Q

What vitamins are essential for hematopoiesis?

A

B vitamins: B9, B12, B6

38
Q

What is folate?

Where do you find folate?

Why is it important?

What decreases folate absorption and reabsorption?

A

Folate/Folic acid is vitamin B9

Most folate is present in green leafy vegetables & other sources as “Polyglutamic Folic Acid”

Converted to the “Monoglutamic Folic Acid” by folate hydrolase before being absorbed

Folate is an important methyl group donor

Folate and its derivatives are needed for nucleotide synthesis (purines and dTMP synthesis) & is important for dividing cells during rapid growth. E.g. Erythropoiesis, Pregnancy and Infancy

Important in hematopoiesis

39
Q

What are some clinical concerns with folic acid deficiency?

A

Megaloblastic anemia. due to the insufficient nucleotides (purines and dTMP) for DNA replication in erythropoiesis and hematopoiesis.

Neurotube defects (NTDs) such as spina bifida and anencephaly: Peri conceptional use of 400 μg/day folic acid (via food fortification and/or folate supplements) decreases the risk of neural tube defects by 70%. Please note that NTDs are multifactorial diseases. Folate deficiency combined with genetically susceptible individuals increase the risk of NTDs; however, the risk cannot be eliminated by folate supplements.

Women who take folic acid during the first four to eight weeks of pregnancy may reduce their child’s risk of the most serious form of autism, suggests a Norwegian study

Cancer: Low folate intake increases risk of colon cancer and breast cancer (the latter is seen in women who drink alcohol.)
Too much folate (>1000 μg/day) appears to increases risk of colorectal cancer (Older people have slow growing cancers that may grow faster with extra folate).
22

40
Q

What is vitamin B12?

A

Compounds with vitamin B12 activity are called cobalamins.

The richest dietary sources of vitamin B12 are meat, eggs, dairy products and liver. Vitamin B12 is made by bacteria and is stored in meat and animal products; it is NOT found in plants.

It takes 20 years to deplete even if the diet is deficient in vitamin B12. Thus, vitamin B12 deficiency is not typically caused by dietary deficiency

Vegans may be at risk

41
Q

What is the path of vitamin B12 absorption?

A

Mouth: R-binder release

Stomach: pepsin and intrinsic factor

Duodenum: B12/IF binding

Ileum: B12/IF endocytosis

Blood circulation: B12/Transcobalamin II

42
Q

What is vitamin B6?

What is it used for?

A

Vit B6 is a collective term for pyridoxine, pyridoxal and pyridoxamine.

Serve as precursors for pyridoxal phosphate which has multiple roles:
•Energy metabolism: co-enzyme for glycogen phoshorylase
•Hematopoiesis: co-enzyme of ALA-S1 & ALA-S2, rate-limiting enzymes of heme biosynthesis pathways.
•Amino acid metabolism: co-enzyme for several enzymes

43
Q

What happens with vitamin B6 deficiency?

A

dietary deficiency is rare, may occur in alcoholics (50%). It manifests as sideroblastic anemia because of the inability to synthesize heme

44
Q

What are the effects of excess vitamin B6?

A

The UL of vitamin B6 is set at 100 mg/dL. Excess B6 (consumption of 500 mg/day for extended periods of time) may cause a toxic neuropathy including trouble walking.

45
Q

What is vitamin B1?

What is it used for?

A

Thiamine

Thiamine pyrophosphate: biologically active form of Vitamin B1. TPP is a coenzyme for :
• Hexose monophosphate (HMP) shunt transketolase reaction
• Two dehydrogenase reactions:
• Pyruvate DHC complex (PDHC)
• α-Ketoglutarate DHC (TCA cycle)

Thiamine has a high turn-over rate. Thus, a continuous dietary supply is necessary. Deficiency can occur after 7 days of thiamine-free diet. Deficiency:↓ ATP production & impaired cellular function.

46
Q

What is Beriberi?

A

A severe thiamine-deficiency syndrome

  • Beriberi means “I can’t, I can’t”.
  • Reduced ATP production primarily affects the nervous and cardiovascular systems and results in extreme weakness.
  • Found in areas where polished rice is the major component of the diet.
  • Infantile Beriberi: nursing infants whose mothers are deficient in thiamine are severely affected
  • Adult beriberi is characterized by dry skin, irritability, disordered thinking, and progressive paralysis
47
Q

What is Wernicke-Korsakoff Syndrome?

A

WKS is a mutifactorial disease. The syndrome only manifests in genetically susceptible individuals when they are also thiamine deficient. Neurological symptoms include ataxia (inability to coordinate voluntary muscular movements), ophthalmoplegia (eye paralysis) and memory loss.

In the US, thiamine deficiency is seen primarily in association with chronic alcoholism due to:

  1. Dietary insufficiency
  2. Impaired intestinal absorption of thiamine.
    (Distilled Spirits Council proposed fortifying whiskey with thiamine)

Treatments for both Beriberi and WKS:
WKS and Beriberi are considered medical emergencies and are treated with 100 mg thiamine (IM or IV). Patients respond in several hours. Death may ensue if not treated.

48
Q

What is vitamin B2?

What is it used for?

Is it a common deficiency?

A

Riboflavin is used to form two coenzymes used in oxidation-reduction reactions:

FMN: Flavin mononucleotide: Riboflavin + phosphate group
FAD: Flavin adenine dinucleotide: FMN + AMP

25% of dietary riboflavin comes from milk and milk products.

Riboflavin has a limited solubility and is light sensitive.

Deficiency is rare in the US except in alcoholics. Alcohol inhibits the digestion and absorption of riboflavin.

There is little evidence that a deficiency of riboflavin is associated with acute or chronic diseases.

49
Q

What is vitamin B3?

What is it used for?

A

Niacin is used to form coenzymes required in redox reactions

NAD+ : Nicotinamide adenine dinucleotide

NADP+: Nicotinamide adenine dinucleotide phosphate

Humans can synthesize up to two thirds of their niacin needs from dietary tryptophan, an essential amino acid.

Clinical Note: Niacin (at 100 times RDA or ~1.5g/day) strongly inhibits lipolysis in adipose tissue, ↓ plasma VLDL and LDL & ↑ HDL. Used for the treatment of hyperlipidemia.

50
Q

What is Niacin deficiency?

A

Pellagra (raw skin)

Pellagra develops in 1 to 2 months when consuming a diet low in both niacin and tryptophan (e.g. corn based meals).

Niacin in many cereal grains is present in an unavailable form; it is covalently linked to lysine residues in proteins called niacytin. E.g. Corn-based diets are low in both niacin and tryptophan.

Pellagra is a chronic wasting disease characterized by the four-D’s (Dermatitis, Diarrhea, Dementia, and eventually Death).

Mental changes include fatigue, insomnia and apathy which maybe due to insufficient tryptophan for the synthesis of serotonin, as well as a reduced energy metabolism.

Treatment produces prompt response within 24 hours.

Today, pellagra is seen in India, parts of Africa and China.

51
Q

What is vitamin B5?

What is it used for?

A

Panthothenic acid is used to form coenzyme A (CoA).

A deficiency in panthothenic acid has never been reported because it is so widespread in food (pan means “everywhere”)

52
Q

What is vitamin B7?

What is it used for?

Is it a common deficiency?

A

A coenzyme for carboxylation reactions

Biotin deficiency is very rare as it is found in many foods and 50% of biotin is made by intestinal bacteria.

Occurs as the free vitamin or attached to lysine residues of proteins (biocytin). This is similar to niacytin.

Unlike niacytin, humans are able to hydrolyze biocytin, releasing biotin for absorption. It is catalyzed by biotinidase in the small intestine.

Biotinidase deficiency is screened in all newborns in AZ.

Avidin, a heat labile protein in egg white, can bind biotin strongly and prevent its absorption. Deficiency only occurs after several months of eating ~2 dozen raw egg whites per day.

53
Q

When might vitamin supplements be necessary?

A

Premenopausal Women: Women who might become pregnant, prevent neural tube defects

Alcoholics: People who consume more than two alcoholic drinks/day.

Elderly: Elderly have a decreased absorption of B12, decreased vitamin D synthesis and often have a low caloric diets.

Dieters: Low caloric diets (<1200 kcal/day) often seen in the elderly and dieters (not enough vitamins in low calorie diets)

Vegans require vitamin B12, no meat

Individuals living north of the 35th parallel: Need supplemental vitamin D in the winter

Individuals who consumes little to no fruit and vegetables

The advice on Vitamins for the general population on a normal balanced diet is that supplementation is unnecessary.

Vitamins cannot compensate for risks associated with smoking, obesity or inactivity

Biochem Exam 2 (7 decks)

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