Vitamin B2 (Riboflavin) and Vitamin B3 (Niacin)

Mechanism

⚡ Vitamin B2 (Riboflavin)

• Coenzyme derivatives: Flavin mononucleotide (FMN) and Flavin-adenine dinucleotide (FAD).
• Function: Electron transporters coupled to dehydrogenases in the Krebs Cycle and the cellular respiratory chain.
• Its deficiency is associated with angular cheilosis, painful glossitis and mucosal hyperemia.

🧬 Vitamin B3 (Niacin / Nicotinic Acid)

• Coenzyme derivatives: Nicotinamide-adenine dinucleotide (NAD) and its phosphorylated form (NADP).
• Function: Cofactor in oxidation-reduction reactions in glycolysis, Krebs Cycle and lipid synthesis.
• Its moderate endogenous synthesis is carried out from dietary tryptophan.

Biochemical pathways of niacin

The endogenous synthesis of niacin dinucleotides requires a regular protein intake. From 60 mg of dietary tryptophan, the liver cell can synthesize 1 mg of niacin equivalent through the kynurenine pathway, which is dependent on vitamins B2 and B6.

The reduced forms NADH and NADPH act as high-energy electron donors:

NAD⁺ acts mainly in catabolic oxidative reactions of mitochondrial degradation, while NADPH derived from the pentose phosphate pathway acts as a critical cellular reductant in anabolic biosynthetic pathways (such as the synthesis of fatty acids and cholesterol) and in the regeneration of mitochondrial reduced glutathione.

The GPR109A Receptor and the Rubicundez Effect (Niacin Flush)

The administration of niacin in high pharmacological doses as a lipid-lowering agent (> 1.5 g/day) induces a transient cutaneous vasodilation known as flush. This phenomenon occurs after the binding of nicotinic acid to its membrane G protein-coupled receptor, GPR109A, located in epidermal Langerhans cells and skin macrophages.

The activation of the receptor stimulates phospholipase A2, inducing the massive production of Prostaglandin D2 (PGD2) and Prostaglandin E2 (PGE2), which cause immediate dermal vasodilation with heat and intense facial itching. Prevention guideline: Coadministration of 325 mg of acetylsalicylic acid (Aspirin) 30 minutes before niacin prevents redness by inhibiting epidermal COX-1.

Indicators and dose

Clinical Indications and Clinical Syndromes

• Treatment of Pellagra (Vitamin B3 Deficiency): Classic systemic disease characterized by the clinical triad of the 3 "D": Dermatitis (symmetrical hyperkeratotic eruptions exposed to sunlight, known as "Casal's collar"), Diarrhea (mucosal atrophy due to impaired epithelial turnover) and Dementia (cortical metabolic failure).
• Treatment of Hyperlipidemia: Niacin decreases the secretion of VLDL by the liver, secondarily reducing serum levels of LDL and triglycerides, and substantially increasing HDL cholesterol by decreasing the clearance of apolipoprotein A-I.