Water Soluble Vitamins Flashcards
(51 cards)
1
Q
vitamins
- definition
- sources
A
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
2
Q
vitamins involved in blood formation/clotting
A
vit B-6
vit B-12
folate
vit K
3
Q
vitamins involved in protein/aa metabolism
A
vit B-6
vit B12
folate
vit C
choline (not true vitamin)
riboflavin (indirect)
4
Q
vitamins involved in antioxidant defenses
A
vit E
vit C
carotenoids
riboflavin (indirect)
5
Q
vitamins involved in gene expression
A
vit A
vit D
6
Q
vitamins involved in bone health
A
vit A
vit D
vit K
vit C
7
Q
vitamins involved in energy metabolism
A
thiamin
riboflavin
niacin
pantothenic acid
biotin
vit B-12
8
Q
vitamins vs carbs/fats/proteins
A
- both organic
differences
- no calories
- micronutrients
- not present in large quantities in food
9
Q
bioavailability and factors that affect it
A
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
10
Q
general process of digestion/abs of water-soluble vitamins (and exceptions)
A
- digestive enzymes/low pH in stomach: hydrolysis of vitamins from bound protein complexes
- 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
11
Q
water-soluble vitamins vs fat-soluble vitamins
A
- 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
- storage
- fat-soluble vits are stored in liver and adipose tissue
- water-soluble vits arent stored for most part
- 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
12
Q
primary fx of B vitamins
cofactors vs. coenzymes vs prosthetic groups
A
- 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)
13
Q
B vitamin mnemonic
A
the rhythm nearly proved fully contagious
thiamine = B1
riboflavin = B2
niacin = B3
pyridoxine = B6
folate = B9
cobalamin = B12
14
Q
B1
- name
- sources
- absorption
A
thiamine
- 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
15
Q
B1 function
A
-
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?)
16
Q
B1 deficiency and toxicity
A
-
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
17
Q
beri beri
A
- 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
18
Q
B2
- name
- sources
- absorption
A
riboflavin
-
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
19
Q
B2 function
A
- prosthetic groups for enzymes
- FAD, FADH2
- involved in redox reactions (oxphos, glutathione reductase for removing ROS)
20
Q
B2 deficiency and toxicity
A
-
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
-
inflammation of membranes (also occurs with some other B deficits)
-
toxicity
- none reported
21
Q
B3
- name
- sources
- forms/absorption
A
niacin
- 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)
22
Q
B3 function
A
- redox reactions (NAD, NADP) - over 200 rxns
- production and breakdown of glucose, fats, a.a.s, nucletides
23
Q
B3 deficiency and toxicity
A
- 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)
-
occurs in supplementation, like when taken for lowering LDL/triacylglycerol and picking up HDL
24
Q
B6
- name
- sources
- absorption
A
pyridoxine
- 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)
25
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)
26
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)
27
B9
* 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
28
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
29
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
30
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)
31
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)
32
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
33
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)
34
B12
* name
* sources
* forms: synthetic and active
cobalamin
* **sources:** foods of animal origin (produced by bacteria, ex. in cattle rumen), also fortified cereals, soy milk
* **forms**
* ****synthetic: cyanocobalamin
* active: methylcobalamin, deoxyadenosylcobalamin
35
B12 digestion and absorption
UNIQUE
* **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
36
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
37
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
38
B7/biotin
* 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
39
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
40
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
41
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
42
vitamin C
* name
* sources
ascorbic acid
* **sources**: fruits, vegetables
43
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)
44
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
45
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_
46
vitamin C: role in neurotransmitter synth
norepi synthesis requires vitamin C
* explains neurological dysfunction and lassitude seen in scruvy
47
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
48
scurvy
* 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
49
vitamin C toxicity
vit C can be metabolized to oxalic acid
* pt with history of oxalate kidney stones should avoid high doses
50
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
51
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look at and memorize last slide
