Donchenko G V, Kuchmerovskaia T M, Parkhomets P K, Obrosova I G, Klimenko A P, Efimov A S
Ukr Biokhim Zh (1978). 1995 Jan-Feb;67(1):105-11.
Studies of neurotransmitter uptake and release by isolated rats brain cortex synaptosomes demonstrated that [2-14C]serotonin uptake was by 41% lower in streptozotocin-diabetic rats as compared to control. The [U-14C]GABA uptake was considerably elevated. [2-14C]serotonin and [U-14C]GABA release from the neurotransmitter pre-loaded synaptosomes showed significant elevation, especially during the first 3 minutes. Nicotinamide (NAm) administration (200 mg/kg body weight daily, 14 days) to diabetic rats restored synaptosomal serotonin uptake up to control levels, while the GABA uptake tended to decrease in diabetic rats. With this dose of NAm the partial restoration of serotonin and GABA release was achieved. The modulating effect of in vivo administered NAm acts via NAD which binds specifically with synaptic membranes. It has been shown that brain NAD(P)/NAD(P)H decreased while sorbitol level increased in streptozotocin-diabetic rats as compared to control. The NAm administration to diabetic rats is accompanied by the increase of NAD(P)/NAD(P)H and the reduction of brain sorbitol level. Data obtained confirm the important role of NAm in the pathogenesis of diabetic encephalopathies.
对分离的大鼠脑皮质突触体的神经递质摄取和释放的研究表明，与对照组相比，链脲佐菌素诱导的糖尿病大鼠中[2-¹⁴C]血清素摄取降低了41%。[U-¹⁴C]γ-氨基丁酸（GABA）摄取显著升高。从预先加载神经递质的突触体中释放的[2-¹⁴C]血清素和[U-¹⁴C]GABA显示出显著升高，尤其是在最初3分钟内。给糖尿病大鼠施用烟酰胺（NAm）（每日200mg/kg体重，共14天）可将突触体血清素摄取恢复至对照水平，而糖尿病大鼠中的GABA摄取则趋于下降。使用该剂量的NAm可部分恢复血清素和GABA的释放。体内施用的NAm的调节作用通过与突触膜特异性结合的烟酰胺腺嘌呤二核苷酸（NAD）起作用。已表明，与对照组相比，链脲佐菌素诱导的糖尿病大鼠中脑NAD(P)/NAD(P)H降低，而山梨醇水平升高。给糖尿病大鼠施用NAm会伴随着NAD(P)/NAD(P)H的增加和脑山梨醇水平的降低。获得的数据证实了NAm在糖尿病性脑病发病机制中的重要作用。
