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链脲佐菌素诱导的糖尿病中坐骨神经脂蛋白脂肪酶减少,胰岛素可使其恢复正常。

Sciatic nerve lipoprotein lipase is reduced in streptozotocin-induced diabetes and corrected by insulin.

作者信息

Ferreira L D M C-B, Huey P U, Pulford B E, Ishii D N, Eckel R H

机构信息

University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.

出版信息

Endocrinology. 2002 Apr;143(4):1213-7. doi: 10.1210/endo.143.4.8723.

Abstract

The metabolic abnormalities underlying the cause of diabetic neuropathy have been the subject of much debate. Lipoprotein lipase (LPL) is a 56-kDa enzyme produced by several tissues in the body and has recently been shown in vitro to be expressed in cultured Schwann cells, where it is important in phospholipid synthesis. This suggests a role for LPL in myelin biosynthesis in the peripheral nervous system. The aim of this study was to determine if acute streptozotocin (STZ)-induced diabetes reduces the expression and regulation of sciatic nerve LPL in vivo. Adult Sprague Dawley rats were rendered diabetic via an sc injection of STZ. A decrease in sciatic nerve LPL activity was observed in the STZ-treated rats after just 2 d of diabetes and remained significantly reduced for at least 35 d. The decrease in LPL activity coincided temporally with a drop in motor nerve conduction velocity. Treatment with insulin for 4 d showed a normalization of sciatic nerve LPL activity. These results show that STZ-induced diabetes causes a decrease in LPL activity in the sciatic nerve that, as in other tissues, is reversible with insulin treatment. These data may suggest a role for LPL in the pathophysiology of diabetic neuropathy.

摘要

糖尿病性神经病变病因背后的代谢异常一直是诸多争论的主题。脂蛋白脂肪酶(LPL)是一种由体内多个组织产生的56 kDa酶,最近在体外实验中显示其在培养的雪旺细胞中表达,在磷脂合成中起重要作用。这表明LPL在外周神经系统的髓鞘生物合成中发挥作用。本研究的目的是确定急性链脲佐菌素(STZ)诱导的糖尿病是否会在体内降低坐骨神经LPL的表达和调节。成年Sprague Dawley大鼠通过皮下注射STZ诱导糖尿病。糖尿病仅2天后,在STZ处理的大鼠中观察到坐骨神经LPL活性降低,并且至少35天内一直显著降低。LPL活性的降低在时间上与运动神经传导速度的下降相吻合。胰岛素治疗4天显示坐骨神经LPL活性恢复正常。这些结果表明,STZ诱导的糖尿病导致坐骨神经LPL活性降低,与其他组织一样,胰岛素治疗可使其恢复正常。这些数据可能提示LPL在糖尿病性神经病变的病理生理学中发挥作用。

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