Niacin is the term that is commonly used for nicotinamide and nicotinic acid. It is best known for its role as a component of two active coenzymes NAD and nicoti-namide adenine dinucleotide phosphate (NADP) that play key roles in energy metabolism. The structure of niacin is shown in Figure 7.3. This vitamin can also be made in the body from tryptophan, a relatively common amino acid.
Niacin absorption occurs readily in the intestine. Approximately 25% of niacin is carried through the blood bound to protein. Niacin is easily absorbed by adipo-cytes; however, it is poorly stored in the body, and excess amounts are generally excreted in the urine as niacin and nicotinamide metabolites.
FIGURE 7.3 Vitamin B3 (niacin).
Niacin functions primarily as a constituent of key nucleotide-containing enzymes that play critical roles in oxidation-reduction reactions as well as ATP synthesis and adenosine diphosphate (ADP)-ribose transfer reactions. NAD is converted into NADP in the mammalian liver. NADP can also be converted to NAD. NAD plays a critical role in catabolic reactions, where it transfers the potential free energy stored in micronutrients, such as carbohydrates, lipids, and proteins, to NADH, which is then used to form ATP, the primary energy currency of the cell. NADP-dependent enzymes are preferentially involved in anabolic reactions, such as the synthesis of fatty acids and cholesterol.
Another key role played by NAD is in DNA repair. By serving as an ingredient in the formation of a DNA polymerase (poly [ADP ribose] polymerase, PARP) it plays a critical role in DNA maintenance. It has been suggested that proper repair of DNA damage would require functional PARP and abundant NAD. The current hypothesis is that if a small amount of DNA damage occurs, PARP activity can repair it, whereas, if more DNA damage occurs, a functional PARP would trigger apoptosis (cell death) probably via NAD depletion.
Increased niacin intake has been proposed to be of benefit for a wide variety of disorders, including diabetes, atherosclerosis, arthritis, and cataracts. High doses of niacin have been used to prevent the development of atherosclerosis and to reduce recurrent complications, such as heart attacks and peripheral vascular disease. Niacin is commonly used to lower elevated low-density lipoprotein (LDL) cholesterol and triglyceride levels in the blood and is more effective in increasing high-density lipoprotein (HDL) levels than other cholesterol-lowering medications. Researchers also found that the combination of niacin and the cholesterol-lowering drug Simvastatin (Merck and Company, Whitehouse Station, New Jersey) may slow the progression of heart disease, reducing risk of a heart attack, and even death.20 Although niacin has been shown to boost HDL cholesterol and decrease triglyceride and LDL cholesterol concentrations, there has been some concern that it may raise blood glucose concentrations. In a recent study involving 125 diabetics and 343 controls, it was shown that high doses of niacin (roughly 3000 mg/d) increased blood glucose concentrations in both groups, but hemoglobin A1C concentration (considered a better measure of blood glucose overtime) actually decreased in the diabetics over a 60 week follow-up period.21
It was also suggested in some preliminary studies that an active form of niacin (niacinamide) may improve symptoms of arthritis, including increased joint mobility and a reduced need for anti-inflammatory medications. Researchers22 speculate that dietary niacin may aid in cartilage repair (damage to joint cartilage causes arthritis) and suggest that it may be used safely along with nonsteroidal anti-inflammatory medications to reduce inflammation. It was also suggested that long-term use (at least 3 yr) may slow the progression of arthritis. Niacin, along with other nutrients, is also important for the maintenance of normal vision and the prevention of cata-racts.23 Severe niacin (nicotinic acid)/tryptophan deficiency has historically been associated with the development of pellagra. This disease has four primary symptoms that are often referred to as the 4 "D"s (diarrhea, dermatitis, dementia, and death).
The Food and Nutrition Board has set the tolerable upper intake level (UL) of niacin at 35 mg/d because of high intakes being associated with flushing of the face, arms, and chest. This limit is not meant to apply to patients under a physician's care who are being treated for hypercholesterolemia.8
The best source of niacin is milk. Other sources are organ meats, whole grains, and some vegetables. The 1998 RDAs for niacin for men and women were 16 and 14 mg of NE (niacin equivalents)/d, respectively.8 American women and men consume an average of 700 mg and 1100 mg of tryptophan, respectively, per day, which represents 16 and 24 NE for women and men, respectively.
Niacin's specific role in wound healing has not been established. It is clear that the B vitamins work together to ensure normal energy metabolism and cell division. Niacin is a key player in both of these essential steps of tissue repair.
Biotin (see Figure 7.4) acts as an energy metabolism coenzyme and is necessary for a maintaining a variety of normal functions in the body. Biotin is primarily absorbed from the small intestine; however, it has also been shown to be absorbed via the colon after it is synthesized by enteric flora. Biotin plays an important role in cells as a carbon dioxide carrier, and it has been shown to deliver a carbon molecule that is used in the formation of three-carbon pyruvate and eventually acetyl CoA. This process is vital for keeping the TCA cycle functioning. Biotin also plays critical roles in gluconeogenesis, fatty acid synthesis, and fatty acid and amino acids breakdown. Hymes and Wolf24 proposed that biotin, by binding to histones, may also play a role in DNA replication and transcription.
Biotin is needed for normal growth and the maintenance of healthy hair, skin, nerves, bone marrow, and sex glands. Biotin deficiency symptoms include hair loss and the development of a scaly rash around the mouth, eyes, nose, and genital area. Depression and lethargy as well as numbness and tingling in the extremities have also been observed. Most recently, biotin deficiency has been associated with non-insulin-dependent diabetes mellitus. When these subjects are provided with biotin, there is a significant decrease in fasting blood glucose concentrations. It was proposed that biotin may increase glucose conversion to fatty acids and also may increase insulin secretion.25
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