Pharmacodynamics<unk>  and nicotinamide are both converted into the coenzyme NAD. NAD converts to NADP by phosphorylation in the presence of the enzyme NAD+ kinase. NAD and NADP are coenzymes for many dehydrogenases, participating in many hydrogen transfer processes. NAD is important in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell signaling and DNA repair, and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis. High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency. Activating HCA2 has effects other than lowering serum cholesterol and triglyceride concentrations: antioxidative, anti-inflammatory, antithrombotic, improved endothelial function and plaque stability, all of which counter development and progression of atherosclerosis.<unk>  inhibits cytochrome P450 enzymes CYP2E1, CYP2D6 and CYP3A4.<unk>  produces a rise in serum unconjugated bilirubin in normal individuals and in those with Gilbert's Syndrome. However, in the Gilbert's Syndrome, the rise in bilirubin is higher and clearance is delayed longer than in normal people. One test used to aid in diagnosing Gilbert's Syndrome involves intravenous administration of nicotinic acid<unk>  in a dose of 50 mg over a period of 30 seconds. Pharmacokinetics Both<unk>  and<unk> amide are rapidly absorbed from the stomach and small intestine. Absorption is facilitated by sodium-dependent diffusion, and at higher intakes, via passive diffusion. Unlike some other vitamins, the percent absorbed does not decrease with increasing dose, so that even at amounts of 3-4 grams, absorption is nearly complete. With a one gram dose, peak plasma concentrations of 15 to 30 μg/mL are reached within 30 to 60 minutes. Approximately 88% of an oral pharmacologic dose is eliminated by the kidneys as unchanged<unk>  or nicotinuric acid, its primary metabolite. The plasma elimination half-life of<unk>  ranges from 20 to 45 minutes.<unk> amide is the major form in the bloodstream. In the liver,<unk> amide is converted to storage nicotinamide adenine dinucleotide (NAD). As needed, liver NAD is hydrolyzed to<unk> amide and<unk>  for transport to tissues, there reconverted to NAD to serve as an enzyme cofactor. Excess<unk>  is methylated in the liver to N1-methylnicotinamide (NMN) and excreted in urine as such or as the oxidized metabolite N1-methyl-2-pyridone-5-carboxamide (2-pyridone). Decreased urinary content of these metabolites is a measure of<unk>  deficiency.<unk> , serotonin (5-hydroxytryptamine), and melatonin biosynthesis from tryptophan
Niacin
Folate
Cholic acid
Zinc
Tocopherol
Iron
Pyridoxine
Pantothenic acid