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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >1-methylnicotinamide (MNA) in prevention of diabetes-associated brain disorders.
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1-methylnicotinamide (MNA) in prevention of diabetes-associated brain disorders.

机译：1-甲基烟酰胺（MNA）预防与糖尿病相关的脑部疾病。

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The present study has been designed to establish the potential benefits from 1-methylnicotinamide (MNA) treatment on brain disorders associated with type 1 diabetes. All experiments were carried out after 6 weeks of streptozotocin-induced diabetes (60 mg/kg of body weight, i.p.) in male Wistar rats treated for 5 weeks with or without MNA (100 mg/kg of body weight, per os in drinking water) after 1 week of diabetes induction. Diabetes was shown to reduce monoamine neurotransmitter serotonin transporters activity, as assessed by significant inhibition of [2-(14)C]serotonin uptake, that was accompanied by elevation of spontaneous mediator release in rat brain synaptosomes. Treatment with MNA slightly attenuated diabetes-induced changes in brain serotoninergic system. The precise mechanism underlying MNA action on central serotonin neurotransmission is not known, but appears to be linked to metabolic and signalling pathways involved in controlling synaptic function rather than being associated with direct modulation of serotonin transporters. In particular, MNA action was associated with its partial normalizing effects on such biochemical indices of neuropathy development as decrease in synaptosomal Na(+),K(+)-ATPase activity and plasma membrane depolarization of synaptic endings. Elevated sorbitol formation in brain and NAD(+) deficits resulted from diabetes as major metabolic imbalances were remarkably countered by MNA treatment. However, diabetes-induced decrease in cytosolic NAD(+) to NADH ratio in brain remained unchanged. Notably, MNA supplementation to diabetic rats caused a slight lowering effect on blood glucose level. Accordingly, our findings indicate that neuroprotective properties of MNA are linked to modulation of synaptic activity through multiple mechanisms. In conclusion, we suggest that 1-methylnicotinamide might be a useful agent for treating brain failures related to diabetes.
机译：本研究旨在确定1-甲基烟酰胺（MNA）治疗对与1型糖尿病相关的脑部疾病的潜在益处。在由链脲佐菌素诱发的糖尿病（60 mg / kg体重，腹膜内）6周后，对雄性Wistar大鼠在饮用水中口服或不口服MNA（100 mg / kg体重，口服）的5周进行所有实验）诱导糖尿病1周后。通过显着抑制[2-（14）C]血清素摄取，并伴随大鼠脑突触体中自发介质释放的升高，评估表明糖尿病降低了单胺神经递质血清素转运蛋白的活性。 MNA的治疗可稍微减轻糖尿病引起的脑5-羟色胺能系统的变化。 MNA对中央5-羟色胺神经传递作用的确切机制尚不清楚，但似乎与参与控制突触功能的代谢和信号通路有关，而不是与5-羟色胺转运蛋白的直接调节有关。特别是，MNA作用与其对神经病发展的生化指标的部分正常化作用相关，如突触体Na（+），K（+）-ATPase活性的降低和突触末端的质膜去极化。 MNA治疗可明显抵抗主要的代谢失衡，从而导致糖尿病引起的脑内山梨醇形成升高和NAD（+）缺乏症。但是，糖尿病引起的脑中胞质NAD（+）与NADH比率的降低保持不变。值得注意的是，向糖尿病大鼠补充MNA会对血糖水平产生轻微的降低作用。因此，我们的发现表明，MNA的神经保护特性与通过多种机制调节突触活性有关。总之，我们建议1-甲基烟酰胺可能是治疗与糖尿病有关的脑衰竭的有用药物。

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