Niacin (B3) Flashcards

1
Q

what are the multiple molecules that make up Niacin (B3)?

A
  • nicotinic acid
  • nicotinamide
  • nicotinamide nucleotides
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2
Q

what are the active forms of niacin (B3)?

A

NAD(H), NADP(H) – nicotinamide nucleotides

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3
Q

what does NAD stand for?

A

nicotinamide ADP-ribose

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4
Q

how does NAD/NADP change to NADH/NADPH?

A

hydride ion (H-) attaches to the molecule

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5
Q

what two of the three molecules that make up niacin are absorbed in the small intestine and transported through circulation to tissue cells?

A

nicotinic acid and nicotinamide

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6
Q

what are the three structures that make up NAD?

A

nicotinamide, ribose, and adenosine

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7
Q

what are the sources of niacin in the diet?

A
  • nicotinamide & NAD+/NADPH: fish and meats
  • nicotinic acid: plants
  • supplements are nicotinamide
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8
Q

how are niacin sources from the diet synthesized?

A

via tryptophan

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9
Q

how is niacin digested, absorbed, transported and stored in the body?

A
  1. NAD/NADP are hydrolyzed in the intestine to make nicotinamide (free form)
  2. nicotinic acid and nicotinamide (free form) are absorbed in the small intestine (via sodium-dependent, carrier-mediated diffusion or by passive diffusion)
  3. nicotinic acid and nicotinamide (free form) are then transported in the blood and move across cell membranes via simple diffusion
  4. NAD(P) is then synthesized from the free form in the liver (or other tissues)
  5. excess NAD(P) is converted back to the free form as storage and available for transport to other tissues when needed
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10
Q

what are the functions and mechanisms of the coenzyme form of niacin?

A
  • oxidative reactions
  • reductive biosynthesis
  • electron donor
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11
Q

what are the functions and mechanisms of the non-coenzyme form of niacin?

A
  • donor of ADP-ribose for protein modification
  • formation of cyclic ADP-ribose
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12
Q

what are the mechanisms of action of NAD+?

A
  • electron acceptor (2e and H+ or hydride H-)
  • de-hydrogen reactions (dehydrogenases)
  • oxidative catabolism and electron transport chain to generate ATP (TCA cycle, glycolysis, beta-oxidation) – good for cell and DNA growth
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13
Q

what are the mechanisms of action of NADPH?

A
  • electron donor
  • reducing agents in reductive biosynthesis (reductases)
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14
Q

how is NADPH generated?

A

via glucose 6-phosphate dehydrogenases in pentose-phosphate pathway

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15
Q

what is the common niacin deficiency and how is it caused?

A
  • pellagra “rough skin”: lack of nicotinic acid or its precursor tryptophan in the diet
  • causes: poor nutritional intake, medication, malabsorptive conditions/disorders
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16
Q

what are the 4 D’s severe symptoms of pellagra?

A

dermatitis, dementia, diarrhea, and death

17
Q

what are the outcomes of large dosages of niacin?

A
  • treat hypercholesterolemia
  • lowering serum LDL and VLDL lipoproteins
  • increase HDL lipoproteins
18
Q

what are the common signs of toxicity of niacin?

A
  • flushing/redness
  • GI problems (heartburn, nausea, vomiting)
  • liver injury
  • glucose intolerance (elevated levels)
19
Q

how do we find the nutritional status of niacin in the body?

A
  • measurement of urinary metabolites
  • erythrocyte NAD concentrations
20
Q

what is the non-redox role of NAD+?

A

serves as a donor of adenosine diphosphate ribose (ADP-ribose) for posttranslational modification of proteins or formation of cyclic ADP-ribose

21
Q

what are the key enzymes niacin is involved with?

A
  • NADH dehydrogenase
  • glyceraldehyde-3-phosphate dehydrogenase
22
Q

what physiological processes is niacin involved with?

A
  • electron transport chain
  • cholesterol and fatty acid synthesis