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低分子量壳聚糖可预防低剂量链脲佐菌素诱导的小鼠缓慢进展性糖尿病的发展。

Low molecular weight chitosan prevents the progression of low dose streptozotocin-induced slowly progressive diabetes mellitus in mice.

作者信息

Kondo Y, Nakatani A, Hayashi K, Ito M

机构信息

Laboratory of Analytical Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan.

出版信息

Biol Pharm Bull. 2000 Dec;23(12):1458-64. doi: 10.1248/bpb.23.1458.

DOI:10.1248/bpb.23.1458
PMID:11145178
Abstract

The present study was designed to clarify the effect of low molecular weight (LMW) chitosan (chitosan lactate, average MW: 20000) on the progression of slowly progressive non-insulin-dependent diabetes mellitus (NIDDM) induced by a single i.p. injection of low dose (100 mg/kg) streptozotocin (STZ) to 8-week-old male ICR mice. The non-fasting serum glucose levels of STZ-treated control mice continued to rise throughout the experimental period until 23 weeks after STZ treatment. The 0.2% or 0.8% chitosan (water solution), given as drinking water from prediabetic stage (2 weeks after STZ treatment), markedly prevented the time course-related rise of serum glucose levels of diabetic mice. In addition, the reduction of relative numbers of insulin-immunoreactive cells (beta-cells) in the islets of diabetic mice at 24 weeks after STZ treatment was markedly prevented by 0.2% or 0.8% chitosan administration. However, the progression of hyperglycemia in diabetic mice was not affected by 0.2% glucosamine, a monosaccharide of chitosan. The glucose levels of normal mice were not affected by 0.8% chitosan administration. When 0.2% chitosan administration was stopped at 20 weeks, these animals had still maintained significantly lower serum glucose levels, compared to control animals, even at 5 weeks after stopping the administration. These results indicate that LMW chitosan prevents the progression of low dose STZ-induced slowly progressive NIDDM.

摘要

本研究旨在阐明低分子量(LMW)壳聚糖(乳酸壳聚糖,平均分子量:20000)对8周龄雄性ICR小鼠单次腹腔注射低剂量(100mg/kg)链脲佐菌素(STZ)诱导的缓慢进展性非胰岛素依赖型糖尿病(NIDDM)进展的影响。STZ处理的对照小鼠的非空腹血清葡萄糖水平在整个实验期内持续升高,直至STZ处理后23周。从糖尿病前期阶段(STZ处理后2周)开始以饮用水形式给予0.2%或0.8%壳聚糖(水溶液),可显著阻止糖尿病小鼠血清葡萄糖水平随时间的升高。此外,在STZ处理后24周时,给予0.2%或0.8%壳聚糖可显著阻止糖尿病小鼠胰岛中胰岛素免疫反应性细胞(β细胞)相对数量的减少。然而,糖尿病小鼠高血糖的进展不受壳聚糖单糖0.2%氨基葡萄糖的影响。给予0.8%壳聚糖对正常小鼠的血糖水平没有影响。当在20周时停止给予0.2%壳聚糖时,即使在停止给药5周后,与对照动物相比,这些动物的血清葡萄糖水平仍显著较低。这些结果表明,低分子量壳聚糖可阻止低剂量STZ诱导的缓慢进展性NIDDM的进展。

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