Department of Physiology, Institute of Basic Medical Sciences, China Medical University, Shenyang, China.
Pharm Biol. 2013 Jan;51(1):8-12. doi: 10.3109/13880209.2012.697175. Epub 2012 Sep 12.
Recent ecological evidence has showed a lag-correlation between the prevalence of diabetes and consumption of niacin (nicotinamide and nicotinic acid) in the US. Nicotinamide has been demonstrated to induce insulin resistance due to excess reactive oxygen species and methyl depletion, whereas the effect of nicotinic acid is poorly understood.
To examine the mechanism of the effect of nicotinic acid on glucose metabolism.
Rats were injected with different cumulative doses of nicotinic acid (0.5, 2, 4 g/kg) and nicotinamide (2 g/kg). A glucose tolerance test was given 2 h after the final injection. The role of methyl consumption and reactive oxygen species generation were evaluated by measuring N(1)-methylnicotinamide and hydrogen peroxide.
Cumulative doses of nicotinic acid produced a dose-dependent increase in the plasma levels of N(1)-methylnicotinamide and hydrogen peroxide, which was associated with a decrease in liver and skeletal muscle glycogen levels. At the same dosage (2 g/kg), in comparison with nicotinamide, nicotinic acid was weaker in raising plasma N(1)-methylnicotinamide levels (0.7 ± 0.11 µg/mL vs. 4.69 ± 0.24 µg/mL, P < 0.001), but stronger in increasing plasma hydrogen peroxide levels (1.88 ± 0.07 µmol/L vs. 1.55 ± 0.05 µmol/L, P < 0.001). Moreover, nicotinamide, unlike nicotinic acid, did not reduce liver glycogen levels.
This study suggested that excessive nicotinic acid, like nicotinamide, might induce methyl consumption, oxidative stress and insulin resistance. Long-term consumption high niacin may increase the risk of type 2 diabetes.
最近的生态学证据表明，美国糖尿病的流行与烟酰胺（烟酰胺和烟酸）的消耗之间存在滞后相关。已经证明烟酰胺由于过多的活性氧和甲基耗竭而导致胰岛素抵抗，而烟酸的作用则知之甚少。
研究烟酸对葡萄糖代谢的影响机制。
向大鼠注射不同累积剂量的烟酸（0.5、2、4 g/kg）和烟酰胺（2 g/kg）。最后一次注射后 2 小时进行葡萄糖耐量试验。通过测量 N(1)-甲基烟酰胺和过氧化氢来评估甲基消耗和活性氧生成的作用。
烟酸的累积剂量导致血浆 N(1)-甲基烟酰胺和过氧化氢水平呈剂量依赖性增加，这与肝和骨骼肌糖原水平降低有关。在相同剂量（2 g/kg）下，与烟酰胺相比，烟酸在提高血浆 N(1)-甲基烟酰胺水平方面较弱（0.7±0.11µg/mL 与 4.69±0.24µg/mL，P<0.001），但在增加血浆过氧化氢水平方面较强（1.88±0.07µmol/L 与 1.55±0.05µmol/L，P<0.001）。此外，与烟酸不同，烟酰胺不会降低肝糖原水平。
本研究表明，过量的烟酸，如烟酰胺，可能会导致甲基消耗、氧化应激和胰岛素抵抗。长期摄入高烟酸可能会增加 2 型糖尿病的风险。
