McGrowder Donovan, Ragoobirsingh Dalip, Brown Paul
Department of Pathology, University of the West Indies, Kingston 7, Jamaica, West Indies.
J Biosci. 2006 Sep;31(3):347-54. doi: 10.1007/BF02704107.
There is increasing evidence that endogenous nitric oxide (NO) influences adipogenesis, lipolysis and insulin-stimulated glucose uptake. We investigated the effect of NO released from S-nitrosoglutathione (GSNO) and S-nitroso-N-acetylpenicillamine (SNAP) on basal and insulin-stimulated glucose uptake in adipocytes of normoglycaemic and streptozotocin (STZ)-induced diabetic rats. GSNO and SNAP at 0.2,0.5, and 1 mM brought about a concentration-dependent increase in basal and insulin-stimulated 2-deoxyglucose uptake in adipocytes of normoglycaemic and STZ-induced diabetic rats. SNAP at 1.0 mM significantly elevated basal 2-deoxyglucose uptake (115.8+/-10.4% compared with GSNO at the same concentration (116.1+/-9.4%; P less than 0.05) in STZ-induced diabetic rats. Conversely, SNAP at concentrations of 10 mM and 20 mM significantly decreased basal 2-deoxyglucose uptake by 50.0+/-4.5% and 61.5+/-7.2% respectively in adipocytes of STZ-induced diabetic rats (P less than 0.05). GSNO at concentrations of 10 mM and 20 mM also significantly decreased basal 2-deoxyglucose uptake by 50.8+/-6.4% and 55.2+/-7.8% respectively in adipocytes of STZ-induced diabetic rats (P less than 0.05). These observations indicate that NO released from GSNO and SNAP at 1 mM or less stimulates basal and insulin-stimulated glucose uptake,and at concentrations of 10 mM and 20 mM inhibits basal glucose uptake. The additive effect of GSNO or SNAP, and insulin observed in this study could be due to different mechanisms and warrants further investigation.
越来越多的证据表明，内源性一氧化氮（NO）会影响脂肪生成、脂肪分解以及胰岛素刺激的葡萄糖摄取。我们研究了从S-亚硝基谷胱甘肽（GSNO）和S-亚硝基-N-乙酰青霉胺（SNAP）释放的NO对正常血糖和链脲佐菌素（STZ）诱导的糖尿病大鼠脂肪细胞基础和胰岛素刺激的葡萄糖摄取的影响。0.2、0.5和1 mM的GSNO和SNAP使正常血糖和STZ诱导的糖尿病大鼠脂肪细胞基础和胰岛素刺激的2-脱氧葡萄糖摄取呈浓度依赖性增加。在STZ诱导的糖尿病大鼠中，1.0 mM的SNAP显著提高了基础2-脱氧葡萄糖摄取（与相同浓度的GSNO相比为115.8±10.4%，GSNO为116.1±9.4%；P<0.05）。相反，在STZ诱导的糖尿病大鼠脂肪细胞中，10 mM和20 mM浓度的SNAP分别使基础2-脱氧葡萄糖摄取显著降低50.0±4.5%和61.5±7.2%（P<0.05）。在STZ诱导的糖尿病大鼠脂肪细胞中，10 mM和20 mM浓度的GSNO也分别使基础2-脱氧葡萄糖摄取显著降低50.8±6.4%和55.2±7.8%（P<0.05）。这些观察结果表明，1 mM或更低浓度的GSNO和SNAP释放的NO刺激基础和胰岛素刺激的葡萄糖摄取，而在10 mM和20 mM浓度时抑制基础葡萄糖摄取。本研究中观察到的GSNO或SNAP与胰岛素的相加作用可能是由于不同机制，值得进一步研究。
