Water Soluble Vitamins Flashcards Preview

Gastrointestinal System > Water Soluble Vitamins > Flashcards

Flashcards in Water Soluble Vitamins Deck (51):


  • definition
  • sources

organic molecules required to maintian normal growth, devpt, metabolism

  • synthesized by gut bacteria: K, biotin
  • synthesized from precursors
    • cholesterol → vit D
    • Trp → niacin
  • dietary intake essential to meet required amts


vitamins involved in blood formation/clotting

vit B-6

vit B-12


vit K


vitamins involved in protein/aa metabolism

vit B-6

vit B12


vit C

choline (not true vitamin)

riboflavin (indirect)


vitamins involved in antioxidant defenses

vit E

vit C


riboflavin (indirect)


vitamins involved in gene expression

vit A

vit D


vitamins involved in bone health

vit A

vit D

vit K

vit C


vitamins involved in energy metabolism




pantothenic acid


vit B-12


vitamins vs carbs/fats/proteins

  • both organic


  • no calories
  • micronutrients
  • not present in large quantities in food


bioavailability and factors that affect it

amount of a nutrient that is actually absorbed and used by body (vs. amt ingested)

  • efficiency of digestion/transit time in GI tract
    • acid production necessary to release B12 from protein to which it is bound
    • diarrhea decreases transit time/abs
  • method of food prep
  • nutrient source (natural vs synthetic/fortified)
  • previous/simultaneous nutrient consumption


general process of digestion/abs of water-soluble vitamins (and exceptions)

1. digestive enzymes/low pH in stomach: hydrolysis of vitamins from bound protein complexes

2. upper part of small intestine: absorption

  • vit B12 absorbed in ileum

​3. bloodstream: distributed throughout body

  • vit B12 stored

4. kidneys: excreted rapidly (i.e. body has ltd stores of water-soluble vitamins - should be consumed daily)

  • vit B12 stored
  • vit B6 (pyridoxine) stored 


water-soluble vitamins vs fat-soluble vitamins

1. transport

  • fat-soluble vits are stored in chylomicrons, released into lymphatic system, then circulated in blood
  • water-soluble vits are released directly into blood and travel free

2. storage

  • fat-soluble vits are stored in liver and adipose tissue
  • water-soluble vits arent stored for most part

3. excretion/toxicitiy

  • water-soluble vit excesses are monitored and removed by kidneys
  • fat-soluble vitamins are stored, excreted less readily → can develop toxicities more quickly

*vits K and B12 have unique props and so tend not to follow the general rules 


primary fx of B vitamins

cofactors vs. coenzymes vs prosthetic groups

  • B vitamins mostly function as components of coenzymes


  • cofactors: accessory molecultes important for protein/enzyme fx
    • either organic (coenzymes) or inorganic (minerals)
    • coenzymes can either by co-substrates (ex. NAD, NADPH) or prosthetic grups (ex. B12, FAD, heme)


B vitamin mnemonic

the rhythm nearly proved fully contagious

thiamine = B1

riboflavin = B2

niacin = B3

pyridoxine = B6

folate = B9

cobalamin = B12



  • name
  • sources
  • absorption


  • sources: whole grain food (significant; fortified cereals), other nutritious food (sunflower seeds, tuna)
  • absorption
    • needs to be phosphorylated to be active (thiamin pyrophosphate)
    • abs reduced in presence of alcohol
    • abs reduced with folate deficiency
    • found in tissues with high metabolic rate: sk muscle, liver, heart, kidneys, brain


B1 function

  • function
    • energy production: helps convert carbs into energy
    • used as a coenzyme with
      • pyruvate dehydrogenase
      • alpha-ketoglutarate dehydrogenase
      • branched chain alpha-ketoacid dehydrogenase (BCK-DH)
      • LIV a.a. metabolism
      • transketolase (HMP pathway)
    • evidence of thiamine-binding proteins thathave roles in nervous system (regulation of nt release?)


B1 deficiency and toxicity

  • deficiency
    • ​often seen in alcoholics (poor abs, increased excretion in urine; Wernicke Korsakoff syndrome), malnourished/homeless, extreme diets
    • symptoms: poor appetite, irritability, apathy, confusion, weight loss
    • advanced: beri beri (wet-CV system, dry-neurologic system)
  • toxicity
    • ​none reported


beri beri

  • B1/thiamine deficiency
  • dry
    • muscle waiting, puan, numbness/tingling of lower extremities, difficulty walking
    • in alcoholics, can progress to Wernicke-Korsakoff syndrome: encephalopathy and psychosis
  • wet
    • abnormalities in cardiovasc system leading to edema



  • name
  • sources
  • absorption


  • sources: milk/milk products, whole grains [+enriched/fortified grains], liver
    • sensitive to UV light/irradiation, stable to heat
  • absorption
    • circulate bound to albumin or other serum proteins
    • converted to active forms FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide) in cell


B2 function

  • prosthetic groups for enzymes
    • FAD, FADH2 
  • involved in redox reactions (oxphos, glutathione reductase for removing ROS)


B2 deficiency and toxicity

  • deficiency
    • inflammation of membranes (also occurs with some other B deficits)
      • cheilosis: cracks at corners of mouth
      • glossitis: infl of tongue
      • stomatisis: infl of mouth/lips, sensitivity to light
      • seborrheic dermatiti: infl skin condition - flaky white/yellow scales on oily areas (scalp, face, inner ear)
    • bloodshot eyes, sensitivity to bright light
  • toxicity
    • none reported



  • name
  • sources
  • forms/absorption


  • sources: protein rich foods (meat, fish, poultry, PB), mushrooms, asparagus, fortified foods
  • absorption
    • found as nicotinic acid, nicotinamide (major form that circulates in blood)
    • active forms: NAD, NADP (from nicotinic acid, nicotinamide, or Trp)


B3 function

  • redox reactions (NAD, NADP) - over 200 rxns
    • production and breakdown of glucose, fats, a.a.s, nucletides


B3 deficiency and toxicity

  • deficiency seen in alcoholics, corn-based diets without other sources of B3
  • pellagra ("rough skin")
    • initially: fatigue, loss of appetite, weakness, anxiety, irritability, depression, GI probs
    • 4Ds
      • diarrhea
      • dermatitis
      • dementia
      • death
  • toxicity
    • occurs in supplementation, like when taken for lowering LDL/triacylglycerol and picking up HDL
      • niacin sometimes cheap alt for statins
    • get niacin flush and itching (treated with low dose aspirin or ibuprofen)



  • name
  • sources
  • absorption


  • sources: protein rich roods (poultry, meat, fish), starchy vegetables, non citrus fruits
  • absorption
    • found as pyridoxal (found mostly in animal products), pyridoxine and pyridoxamine (found ostly in plants)
    • all are converted to PLP (pyridoxal phosphate, a coenzyme - key for a.a. metabolism)


B6 function

  • transamination reactions (moving amino groups from a.a. to keto acids)
  • deamination reactions
    • amino acid metabolism
    • urea metabolism
  • conversion of Trp to niacin
    • implication: B6 deficiency can lead to B3 deficiency!
  • neurotransmitter synthesis (serotonin, dopamine, norepi, histamine)
  • heme synthesis (pyridoxine is coenzyme for ALA synthase in committed step)


B6 deficiency and toxicity

  • deficiency is rare, only in some cases
    • newborns fed formula low in B6
    • women taking oral contraceptives
    • alcoholics
    • can be consequence of drug interactions
      • isoniazid (used to treat TB) binds to B6, induces deficiency
      • penicillamine (used to treat rheumatoid arthritis) depletes pyridoxine → deficiency
    • symptoms: cheliosis, glossitis, pellagra-like dermatitis, depression, confusion (note overlap with B3 symptoms! think B6 fx)
  • toxicity
    • used pharmacologically to treat carpal tunnel, PMS, asthma, depression, pregnancy nausea, diabetic neuropathy
    • HOWEVER, high doses can lead to irreversible nerve damage (sensory damage, difficulty walking, numbness of hands/feet)



  • name
  • sources
  • forms
  • absorption

folate [NOT REFERRED TO BY # (B9)]

  • codependent with cbalamin (B12)
  • sources: dark leafy vegetables (spinach, broccoli, legumes, cirtus fruits), liver, fortified bread/cereal (via folic acid)
  • forms/absorption
    • unlike other B vitamins, many active forms 
    • basic structure: ring structure (pteridine) - PABA bridge molecule (para-aminobenzoic acid) - glutamate
    • usually have multiple glutamates at end of chain (aka polyglutamates)
      • additional Glu are removed in intestine (until only one left) and methyl group is added: methyltetrahydrofolate which is released in circ and delivered to cells
      • in cells, methylterrahydrofolate is inactive, must be converted to active form


how are folates converted from inactive form (methyltetrahydrofolate) to active form in cells?

vitamin B12!!!

  • B12 knocks the methyl off of methyltetrahydrofolate, attaches it to itself
    • B6 - methyl = activated
    • B12 + methyl = activated
    • both are now ready for their roles in synthesis


B9/folate function

  • role in synthesis of DNA, RNA, some a.a.s
    • esp important in rapidly dividing cells (RBCs, epithelial cells, embryonic cells)
  • regen of Met from homoCys


B9/folate deficiency: reasons, main signs


link between B9/B12 deficiency

  • deficiency due to increased demand (during preg), inadequate absorption (Celiac, Crohn's), antifolates (ex. methotrexate - leukemia treatment), aldoholism, antacids (hinder abs by increasing pH of upper int)
    • macrocytic anemia
      • weakness, fatigue, headache, palpitations, SOB
  • tx? supplement BUT **WARNING**
    • folate supp can reverse anemia, but might mask symptoms of a B12 deficiency - might think you're getting better and still have neuro damage
    • either give folic acid + B12 or methylmalonic acid test (accumulation = B12 def)


folate and birth defects

  • folate deficiency associated with neural tube defects
    • spina bifida (neural tube not fully closed)
    • anencephaly (brain/skull underdeveloped)
  • folate supplementation advised for women planning to be pregnant (folic acid before/during pregnancy)


folate and heart disease

  • homocysteine is an independent risk factor for atherosclerosis
    • increased homoCys due to folate deficiency can be a marker for increased risk of CVD
  • smokers might benefit from folic acid supplementation → reduced risk of stroke


B9/folate toxicity

excessive consumption of folic acid as supplement could mask a potential B12 deficiency

  • would take care of expected anemia, BUT could lead to progression of neurological deterioration (if B12 def undetected as a result)



  • name
  • sources
  • forms: synthetic and active


  • sources: foods of animal origin (produced by bacteria, ex. in cattle rumen), also fortified cereals, soy milk
  • forms
    • synthetic: cyanocobalamin
    • active: methylcobalamin, deoxyadenosylcobalamin


B12 digestion and absorption


  • salivary glands: release R protein
    • R protein and protein-bound B12 move to stomach
  • stomach: 
    • B12 is released from its binding protein
    • B12 binds to R protein
    • parietal cells release IF (intrinsic factor)
    • R-bound B12 and IF move to duodenum
  • duodenum: pancreatic enzymes clear R-protein-bound B12, allowing B12 to bind to IF
    • IF-bound B12 moves through intestines to ileum
  • ileum: IF receptors allow internalization of B12 to ileal epithelial cells
    • in epithelial cells, B12 is released from IF
    • B12 binds to transcobalamin II, moves to liver via hepatic circulation
    • due to enterohepatic circ, can be good for several years


B12 functions

**B12 and folate depend on each other for activation**

  • regeneration of Met, synthesis of DNA, synthesis of RNA
  • metabolism of odd-numbered FAs and many a.a.s
  • helps maintain nerve cells


B12 deficiency

  • deficiency
    • malnutrition (ex. vegan diet w no supplementation)
    • issues with absorption
      • pernicious anemia: damage to parietal cells via autoimmune disease: decrease in IF
      • atrophic gastritis with aging, damages cells of stomach: low HCl and IF production
      • decreased gastric acid production (antacids/proton pump inhibitors)
      • terminal ileum removal (site of B12 abs)
  • symptoms
    • megaloblastic anemia
    • nerve damage
    • painful, swollen tongue



  • name
  • functions
  • deficiency
  • toxicity

biotin [not known as B7]

  • function
    • coenzyme in carboylation rxn
    • needed by ABC carboxylases (ATP, biotin, CO2)
    • req for metabolism of carbs, fats, proteins
  • deficiency
    • rare
    • sometimes seen as biotinidase deficiency (enzyme needed to recycle active form of biotin) : skin rash, hair loss, convulsions, impaired growth
    • also seen with excessive consumption of raw eggs : excess avidin (binds biotin v tightly)
  • toxicity
    • none known


biotinidase deficiency

  • inability to recycle biotin
  • inherited: autosomal recessive; part of newborn screening in US
  • symptoms
    • hypotonia (weak muscles), seizures, alopecia (hair loss), eczema, dept delays, lactic aciduria


B5/pantothenic acid

  • sources
  • form
  • functions
  • deficiency/toxicity?

pantothenic acid [not known as B5]

  • sources: meat milk, many veggies
  • form: part of coenzyme A (acyl and acetyl group carrier)
  • function
    • essential for activation of FAs and fat metabolism (synthesis of FAs, triacylglycerol, cholesterol, acetylcholine)
    • cell membrane symthesis
  • deficiencies are rare, toxicity: none known


interactions among B vitamins [3 examples]

  • folate and B12 are dependent on each other for activation
  • FMN (riboflavin, B2) is key for conversion of B6 (pyridoxine) to PLP
  • FMF, PLP, and iron are required for conversion of Trp to niacin (B3)


  • B vitamins are all involved directly or indirectly in energy metabolism
    • sources often have overlaps of B vitamins
  • deficiencies can be linked, with common symptoms (cheilosis, glossitis) and it can be hard to tell what vitamin/deficiency is actually responsible for a symptom



vitamin C

  • name
  • sources

ascorbic acid

  • sources: fruits, vegetables


C functions

  • collagen formation
    • strengthening bones and blood vessels
    • anchoring teeth in gums
    • tissue repair
    • wound healing
  • water soluble antioxidant
  • synthesis of carnitine: key for FA degradation
  • synthesis of neurotransmitters: norepi
  • enhances intestinal abs of non-heme Fe (increases bioavailability of Fe from food)


vitamin C: antioxidant ability

  • vitamin C readily donates electrons to free radicals and ROS
  • protects proteins, nucleic acids, cabs, lipids from oxidative damage
  • vitamin C can be reduced back to its active form


vitamin C: collagen synth

  • used as a cosubstrate/cofactor by two enzymes involved in collagen synthesis
    • prolyl hydroxylase: catalyzes selective mod of Pro → hydryxproline
    • lysyl hydroxylase: catalyzes conversion of Lys → hydroxylysine

vitamin C def leads to nonfunctional collagen in blood vessels and bones


vitamin C: role in neurotransmitter synth

norepi synthesis requires vitamin C

  • explains neurological dysfunction and lassitude seen in scruvy


vitamin C deficiency risk factors

  • urban/poor adults (food deserts/low access to fruits and veg)
  • severe bones/fractures (higher demand for vit C for collagen synth)
  • alcohol and/or smoking



  • ​muscle weakness, jt pain
  • loose teeth, bleeding swollen gums (scorbutic gums)
  • bruised skin, pinpoint hemmorhages (spontaneous internal bleeding - bad blood vessels), impaired wound healing
  • fatigue


vitamin C toxicity

vit C can be metabolized to oxalic acid

  • pt with history of oxalate kidney stones should avoid high doses


vitamin C as medicine

  • doesnt prevent, but can reduce severity of common cold
  • more research needed:
    • might reduce oxidation of LDLs
    • might help reduce risk of cancer/aid in cancer treatment


look at and memorize last slide

look at and memorize last slide