U01.01.076 Vitamin B3

 

Learning Objectives

  • Identify NAD+ and NADP+ as the active forms of Niacin.
  • Explain the de novo synthesis of Niacin from Tryptophan and the required cofactors (B2, B6).
  • Recognize the “3 D’s” of Pellagra and its diverse etiologies.
  • Contrast the side effects of Niacin excess, including prostaglandin-mediated flushing.

1. Biochemical Function & Synthesis

Niacin (Vitamin B3) is essential for energy metabolism. It is a constituent of NAD+ and NADP+, which serve as electron carriers in redox reactions.

  • Synthesis: Derived from the amino acid Tryptophan. This process requires Vitamin B2 (Riboflavin) and Vitamin B6 (Pyridoxine).
  • Therapeutic Use: Used to treat dyslipidemia by decreasing VLDL and significantly increasing HDL.
Memory Hook: NAD is from Niacin (B3 yields ~ 3 ATP).

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2. Deficiency: Pellagra and the “3 D’s”

Severe deficiency leads to Pellagra. While dietary lack is one cause, several other conditions can precipitate this state:

Symptom (The 3 D’s) Clinical Presentation
Dermatitis Hyperpigmentation of sun-exposed areas; Casal necklace (C3/C4 broad collar rash).
Diarrhea Due to atrophy of the columnar epithelium of the GI tract.
Dementia Includes hallucinations and cognitive decline. (The 4th “D” is Death).

Secondary Causes of Pellagra:

  • Hartnup Disease: AR deficiency of neutral amino acid transporters (Tryptophan) in the kidneys and gut.
  • Malignant Carcinoid Syndrome: Increased Tryptophan consumption to synthesize excess Serotonin.
  • Isoniazid (INH) Therapy: Depletes Vitamin B6, which is required for Niacin synthesis.

3. Niacin Excess (Toxicity)

High doses of Niacin used for lipid control can cause significant side effects.

  • Facial Flushing: Induced by Prostaglandins (not histamine). Taking Aspirin 30 minutes before Niacin can prevent this.
  • Metabolic Effects: Can cause hyperglycemia (insulin resistance) and Hyperuricemia (may precipitate Gout/Podagra).

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