The Vitamin Nicotinamide: Translating Nutrition into Clinical Care

Abstract

Nicotinamide, the amide form of vitamin B3 (niacin), is changed to its mononucleotide compound with the enzyme nicotinic acide/nicotinamide adenylyl-transferase, and participates in the cellular energy metabolism that directly impacts normal physiology. However, nicotinamide also influences oxidative stress and modulates multiple pathways tied to both cellular survival and death. During disorders that include immune system dysfunction, diabetes, and aging-related diseases, nicotinamide is a robust cytoprotectant that blocks cellular inflammatory cell activation, early apoptotic phosphatidylserine exposure, and late nuclear DNA degradation. Nicotinamide relies upon unique cellular pathways that involve forkhead transcription factors, sirtuins, protein kinase B (Akt), Bad, caspases, and poly (ADP-ribose) polymerase that may offer a fine line with determining cellular longevity, cell survival, and unwanted cancer progression. If one is cognizant of the these considerations, it becomes evident that nicotinamide holds great potential for multiple disease entities, but the development of new therapeutic strategies rests heavily upon the elucidation of the novel cellular pathways that nicotinamide closely governs.

Nicotinamide Blocks Proliferation and Induces Apoptosis of Chronic Lymphocytic Leukemia Cells through Activation of the p53/miR-34a/SIRT1 Tumor Suppressor Network

“…þ , an essential cofactor in the oxidative phosphorylation chain (1), is a substrate for 4 classes of enzymes (2,3), involved in genomic stability, apoptosis, cell signaling, stress tolerance, and metabolism (4)(5)(6)(7). Among these enzymes, sirtuins catalyze the deacetylation of acetyl-lysine residues by cleaving NAD þ and generating O-acetyl ADP-ribose.…”

The Optimum Conditions of Carboxymethyl Chitosan Synthesis on Drug Delivery Application and Its Release of Kinetics Study

“…In this paper, chitosan is modified into CMC to improve the encapsulation efficiency and release kinetics. Encapsulation efficiency between chitosan and CMC was determined by nicotinamide (NA) as drug model [25][26]. Rate release of nicotinamide from matrix system will be determined by slow release kinetics mechanism [27][28][29][30].…”

Nicotinamide-induced Mitophagy

“…NAM promotes the survival of a variety of cell types, mainly by serving as a source of NAD ϩ (15). One of the known molecular targets of increased NAD ϩ levels is SIRT1, a member of the NAD ϩ -dependent protein deacetylase family (16).…”