Nutri Sci 332 | Exam 3

Function of Vitamin C

Antioxidant, cofactor in the synthesis of collagen,

Absorption of Vitamin C

Active transport via SVCT1 and SVCT2, brush border enzymes. Water soluble so directly into blood

Excretion of Vitamin C

Travels freely in the blood, excess is filtered out by kidneys and removed in urine

Where does a Vitamin C deficiency show up first?

Areas linked to maintaining blood integrity, death by internal bleeding

Diseases associated with Vitamin C deficiency

Scurvy. “First” controlled human trial. Potato cultivation

Vitamin C food sources

Citrus fruits, red bell peppers, broccoli

Who has a higher need for Vitamin C?

Smokers (due to higher oxidant burden)

Vitamin C recommendations

UL » RDA

Symptoms of toxicity of Vitamin C

nausea, cramps, diarrhea

B vitamins

Participate in energy metabolism, water soluble, absorbed in the small intestine, sometimes passive, but most often facilitated or active transport

Function of Vitamin B1

Cofactor for thiamin pyrophosphate (TPP which is vital for energy metabolism and neurotransmitter synthesis)

TPP is the coenzyme in what metabolic pathways?

Pyruvate dehydrogenase, decarboxylation of alpha-keto acids, transketolase activity, neurotransmitter synthesis

Absorption of Vitamin B1

generally active transport via specific transporters

Excretion of Vitamin B1

Travels through blood and generally bound to albumin, not much storage (primarily liver), excreted in the urine

Diseases associated with Vitamin B1 deficiency

Beriberi (wet/dry), and Wernicke-Korsakoff syndrome

Wet Beriberi

Changes in the cardiovascular system, shortness of breath, fast heart rate, leg swelling (edema)

Dry Beriberi

Affects the nervous system - numbness in extremities, confusion, pain. Changes in the peripheral nervous system, primarily neurological (phantom limbs). Essentially the same as Wernicke-Korsakoff syndrome

Thiamin deficiency

Typically a consequence of insufficient food intake to meet energy needs and/or a diet very high in “empty” calories

Who has a higher need of Vitamin B1?

Alcoholics (diet high in empty calories, poor absorption, and increased amounts of excretion) and the homeless

Wernicke-Korsakoff syndrome

Shows up in alcoholics, ataxia (staggering gait), nystagmus (rapid eye movement)

Vitamin B1 food sources

Lean pork chop, soy milk, cornflakes (fortified), squash/acorn, tomato juice

Vitamin B1 recommendations

No established UP, no toxicity symptoms

Function of Vitamin B2

Coenzyme to FMN and FAD (central to redox reactions, energy metabolism, and fatty acid oxidation)

Coenzyme

How we get in our diet

FMN

Integral component of the ETC

FAD (or FADH₂)

Involved in the beta-oxidation of fatty acids, conversion of tryptophan to niacin, reduction of oxidized glutathione by glutathione reductase (used to assess sufficiency status)

Can tell how much someone has based on enzymatic function

Glutathione by glutathione (reaction will proceed as expected, and if not, may be deficient in Vitamin B2)

Absorption of Vitamin B2

In small intestine through active transport and passive diffusion

Excretion of Vitamin B2

Excess is excreted via the urine (large doses turn urine bright yellow)

Where does a deficiency in Vitamin B2 show up first?

Lesions or swelling in and around the mouth

Who has a higher need of Vitamin B2?

Pregnant people, alcoholics and the elderly

Where does a Vitamin B1 deficiency show up first?

Cardiovascular system (edema) and the nervous system (numbness, confusion).

Diseases associated with Vitamin B2 deficiency

Ariboflavinosis, although uncommon since it is usually associated with other deficiencies (B-6, B-12, folate, niacin)

Vitamin B2 food sources

Liver (central metabolic hub), yogurt, milk, cornflakes (fortified), broccoli, and egg

25% of intake is from dairy products and is sensitive to UV light

Vitamin B2

Vitamin B2 recommendations

No UL, no symptoms of toxicity

How are levels of Vitamin B2 assessed?

Glutathione reductase activity in RBCs

Function of Vitamin B3

Cofactors for NAD and NADP (which are essential for central energy metabolism/TCA cycle and biosynthesis)

Turning of TCA cycle produces

Reduced NADH

NADH delivers electrons to the ETC

The movement of electrons drives proton pump and enables synthesis of ATP

Vitamin B3 recommendations

RDA & UL have a 2 fold difference

Absorption of Vitamin B3

Facilitated transport or passive diffusion

NE

“niacin equivalents” (we can make)

Synthesis of Vitamin B3

From tryptophan

Excretion of Vitamin B3

Travels through the blood, not much storage – liver can convert some excess plasma nicotinamide to NAD storage, excreted in the urine

Where does a Vitamin B3 deficiency show up first?

4Ds: Dementia, Diarrhea, Dermatitis, Death

Diseases associated with Vitamin B3 deficiency

Pellagra (the 4Ds)

Vitamin B3 food sources

Chicken breast, tuna (canned in water), liver, cornflakes (fortified), mushrooms

Who has a higher need for Vitamin B3?

Populations relying on untreated corn

Nixtamalization

Address the bioavailability issue in corn, soaks and cooks corn in an alkaline solution which breaks the bonds holding the niacin, releasing it and making it available for absorption by the body

Symptoms of toxicity of Vitamin B3

“Niacin flush” — diluted capillaries and potentially painful tingling sensation

Function of Vitamin B5

Precursor to the synthesis of Acetyl-CoA and acyl-carrier protein, & involved in more than 100 different reactions for lipid, neurotransmitter synthesis

Absorption of Vitamin B5

Exists as the CoA form and must be broken down in the intestine before absorption

Many of the B vitamins are sensitive to heat

Consequence for the bioavailability of vitamins in food

Excretion of Vitamin B5

Circulation in the blood, minimal storage, excretion of excess via kidneys/urine

Where does a Vitamin B5 deficiency show up first?

Very rare, include general failure of all the body’s systems (fatigue, GI distress, neurological symptoms)

Nutrient-drug interaction with Vitamin B5

Estrogen-containing oral contraceptives may increase requirement

Diseases associated with Vitamin B5 deficiency

“Burning feet” syndrome of prisoners of war in Asia during WW2

Vitamin B5 food sources

Beef liver, mushrooms, sunflower seed kernels, fish/trout

Vitamin B5 recommendations

No established UL, no toxicity symptoms

Function of Vitamin B7

Cofactor in metabolic reactions, especially utilization of fats, carbs, or amino acids

Absorption of Vitamin B7

Biotinidase (brush border enzyme) must release it from food proteins before facilitated transport in the small intestine

Excretion of Vitamin B7

Travels through the blood, some storage in liver, excreted in the urine

Where does a Vitamin B7 deficiency show up first?

skin rash, hair loss, neurological impairment

Acetyl-CoA carboxylase

Irreversible step of fatty acid synthesis

Diseases associated with Vitamin B7 deficiency

Biotinidase deficiency is autosomal recessive (enzyme in small intestine may be deficient). Impairs intestinal absorption of biotin

Vitamin B7 food sources

Liver, egg, salmon, yeast

Vitamin B7 recommendations

No established UL, no toxicity symptoms

Function of Vitamin B6

Cofactor of PLP — involved in ~4% of all enzymatic reactions

Absorption of Vitamin B6

Via passive diffusion after being de-phosphorylated

Pyridoxal 5`-phosphate (PLP)

Hemoglobin and amino acid biosynthesis, fatty acid metabolism, glycogen phosphorylase, gluconeogenesis, neurotransmitter biosynthesis. Synthesis of niacin from tryptophan

Excretion of Vitamin B6

Sent out via blood from liver bound to albumin, some storage — liver and also muscle. Excretion of excess via kidneys/urine in the form of 4-pyridoxic acid

Where does a Vitamin B6 deficiency show up first?

Small, pale red blood cells, seborrheic dermatitis (skin), depression (brain), impaired immune function. High cell turnover areas.

Diseases associated with Vitamin B6 deficiency

Uncommon, microcytic hypochromic anemia

Microcytic hypochromic anemia

Small, pale red blood cells due to impaired hemoglobin synthesis

Vitamin B6 recommendations

RDA « UL

Symptoms of toxicity of Vitamin B6

Neurological damage (peripheral neuropathy)

Vitamin B6 food sources

Banana, cornflakes (fortified), tomato juice, watermelon

The plant form of Vitamin B6 in some plant sources

Pyridoxine glucoside appears to be less bioavailable

Who has a higher need for Vitamin B6?

Alcoholics and those over 50 years of age

Function of Vitamin B9

5 coenzyme forms, derivatives of THFA which move around single carbons. Essential for DNA synthesis and repair (crucial for cell division)

Methotrexate

A chemotherapeutic agent that is an antagonist of folate. Can be helpful in the treatment of cancer and rheumatoid arthritis (to stop the proliferation of white blood cells). Folate is commonly prescribed to minimize toxic effects. (Skin cells, white and red blood cells, intestinal lining)

Cofactor forms of Vitamin B9

DHF, THFA

In homocysteine metabolism, Vitamin B9 is

Intermediate between methionine and cysteine

Vitamins B6, B9, and B12

Lower homocysteine in blood

High levels of homocysteine in the blood

Correlated with cardiovascular disease (blood clots, heart attacks, strokes)

Vitamin B9 recommendations

RDA and UL are relatively close

Dietary folate equivalents

Units that express folate needs or intake. Reflects the difference in absorption from food folate vs synthetic folic acid

Absorption of Vitamin B9

Polyglutamates from food are broken down to monoglutamates for absorption in the small intestine through active and passive (at high concentrations) transport

Excretion of Vitamin B9

Circulation in the blood, liver process monoglutamate form to polyglutamate (store a limited amount in liver), enterohepatic circulation where liver incorporates excess folate into bile

Where does a Vitamin B9 deficiency show up first?

Decrease in blood folate, defective DNA synthesis, structure change in some white blood cells, homocysteine concentration rises in the blood

Diseases associated with Vitamin B9 deficiency

Megaloblastic (macrocytic anemia), spina bifida