Nicotinamide riboside: Difference between revisions

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''H. influenza'' depends entirely on salvage of NAD precursors from other cells in its environment.

The identification of Nicotinamide riboside (NR) as an NAD precursor in [[eukaryotes]] developed out of the study of [[pellagra]].~~<ref name="pmid35918544"/>~~ Pellagra was the first disease to be associated with NAD+ deficiency. It was linked to nutritional deficiency by [[Joseph Goldberger]] in 1914, and to deficiency of [[Niacin (substance)|niacin]] ([[Vitamin B3|vitamin B<sub>3</sub>]]) by [[Conrad Elvehjem]] in 1937. NAD+ (then called coenzyme I) was shown to be extremely low in cases of pellagra, and NA and NAM were identified as molecular precursors in rebuilding NAD+ levels. Pellagra is now understood as a severe, chronic depletion of NAD+, which can be treated through diet.

The identification of Nicotinamide riboside (NR) as an NAD precursor in [[eukaryotes]] developed out of the study of [[pellagra]]. Pellagra was the first disease to be associated with NAD+ deficiency. It was linked to nutritional deficiency by [[Joseph Goldberger]] in 1914, and to deficiency of [[Niacin (substance)|niacin]] ([[Vitamin B3|vitamin B<sub>3</sub>]]) by [[Conrad Elvehjem]] in 1937. NAD+ (then called coenzyme I) was shown to be extremely low in cases of pellagra, and NA and NAM were identified as molecular precursors in rebuilding NAD+ levels. Pellagra is now understood as a severe, chronic depletion of NAD+, which can be treated through diet.

Subsequent studies of NAD+ metabolism have identified regulatory pathways used by cells and tissues to maintain NAD+ availability. NAD+ and its precursors nicotinic acid (NA) and nicotinamide (NAM) have been shown to be vital cofactors in cellular [[Redox|oxidation/reduction reactions]] and [[Adenosine triphosphate|ATP]] synthesis. Classic NAD+ synthesis pathways characterized in eukaryotes include an eight-step ''de novo'' pathway from Trp and two pathways using the NAD+ precursors NA and NAM: a three-step NA-based pathway known as the Preiss-Handler pathway; and an NAM-based pathway involving the enzyme [[Nicotinamide phosphoribosyltransferase]] (NAMPT) and the formation of nicotinamide mononucleotide (NMN).

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 ''H. influenza'' depends entirely on salvage of NAD precursors from other cells in its environment.
-The identification of Nicotinamide riboside (NR) as an NAD precursor in [[eukaryotes]] developed out of the study of [[pellagra]].<ref name="pmid35918544"/> Pellagra was the first disease to be associated with NAD+ deficiency. It was linked to nutritional deficiency by [[Joseph Goldberger]] in 1914, and to deficiency of [[Niacin (substance)|niacin]] ([[Vitamin B3|vitamin B<sub>3</sub>]]) by [[Conrad Elvehjem]] in 1937.  NAD+ (then called coenzyme I)  was shown to be extremely low in cases of pellagra, and NA and NAM were identified as molecular precursors in rebuilding NAD+ levels. Pellagra is now understood as a severe, chronic depletion of NAD+, which can be treated through diet.
+The identification of Nicotinamide riboside (NR) as an NAD precursor in [[eukaryotes]] developed out of the study of [[pellagra]]. Pellagra was the first disease to be associated with NAD+ deficiency. It was linked to nutritional deficiency by [[Joseph Goldberger]] in 1914, and to deficiency of [[Niacin (substance)|niacin]] ([[Vitamin B3|vitamin B<sub>3</sub>]]) by [[Conrad Elvehjem]] in 1937.  NAD+ (then called coenzyme I)  was shown to be extremely low in cases of pellagra, and NA and NAM were identified as molecular precursors in rebuilding NAD+ levels. Pellagra is now understood as a severe, chronic depletion of NAD+, which can be treated through diet.
 Subsequent studies of NAD+ metabolism have identified regulatory pathways used by cells and tissues to maintain NAD+ availability. NAD+ and its precursors nicotinic acid (NA) and nicotinamide (NAM) have been shown to be vital cofactors in cellular [[Redox|oxidation/reduction reactions]] and [[Adenosine triphosphate|ATP]] synthesis.  Classic NAD+ synthesis pathways characterized in eukaryotes  include an eight-step ''de novo'' pathway from Trp and two pathways using the NAD+ precursors NA and NAM: a three-step NA-based pathway known as the Preiss-Handler pathway; and an NAM-based pathway involving the enzyme [[Nicotinamide phosphoribosyltransferase]] (NAMPT) and the formation of nicotinamide mononucleotide (NMN).