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醛糖还原酶抑制剂对糖尿病患者红细胞果糖3 - 磷酸和山梨醇3 - 磷酸水平的影响。

Effects of an aldose reductase inhibitor on erythrocyte fructose 3-phosphate and sorbitol 3-phosphate levels in diabetic patients.

作者信息

Hamada Y, Odagaki Y, Sakakibara F, Naruse K, Koh N, Hotta N

机构信息

Third Department of Internal Medicine, Nagoya University School of Medicine, Japan.

出版信息

Life Sci. 1995;57(1):23-9. doi: 10.1016/0024-3205(95)00239-3.

DOI:10.1016/0024-3205(95)00239-3
PMID:7596218
Abstract

Fructose 3-phosphate and sorbitol 3-phosphate are novel metabolites that have been shown to associate with the polyol pathway in animal experiments. Fructose 3-phosphate is of particular interest because of its potent glycation capability as compared with other glycolytic intermediates, e.g., fructose. We observed the effects of treatment with epalrestat, an aldose reductase inhibitor, on their concentrations in erythrocytes from diabetic patients. The levels of both metabolites were significantly higher in diabetic patients than in non-diabetic subjects. A group of patients who had been treated with epalrestat showed significantly lower levels of both metabolites as compared with those untreated. A treatment of three patients with epalrestat for one month resulted in obvious decreases in their concentrations. The results suggest a possible explanation for the preventive effect of an aldose reductase inhibitor on nonenzymatic glycation.

摘要

3-磷酸果糖和3-磷酸山梨醇是新发现的代谢产物,在动物实验中已显示它们与多元醇途径相关。3-磷酸果糖特别引人关注,因为与其他糖酵解中间产物(如果糖)相比,它具有很强的糖化能力。我们观察了醛糖还原酶抑制剂依帕司他对糖尿病患者红细胞中这些代谢产物浓度的影响。糖尿病患者体内这两种代谢产物的水平均显著高于非糖尿病受试者。与未接受治疗的患者相比,一组接受依帕司他治疗的患者体内这两种代谢产物的水平均显著降低。对三名患者使用依帕司他治疗一个月后,其浓度明显下降。这些结果为醛糖还原酶抑制剂对非酶糖化的预防作用提供了一种可能的解释。

相似文献

1
Effects of an aldose reductase inhibitor on erythrocyte fructose 3-phosphate and sorbitol 3-phosphate levels in diabetic patients.醛糖还原酶抑制剂对糖尿病患者红细胞果糖3 - 磷酸和山梨醇3 - 磷酸水平的影响。
Life Sci. 1995;57(1):23-9. doi: 10.1016/0024-3205(95)00239-3.
2
Epalrestat, an aldose reductase ihibitor, reduces the levels of Nepsilon-(carboxymethyl)lysine protein adducts and their precursors in erythrocytes from diabetic patients.依帕司他,一种醛糖还原酶抑制剂,可降低糖尿病患者红细胞中Nε-(羧甲基)赖氨酸蛋白加合物及其前体的水平。
Diabetes Care. 2000 Oct;23(10):1539-44. doi: 10.2337/diacare.23.10.1539.
3
Role of polyol pathway in nonenzymatic glycation.多元醇途径在非酶糖基化中的作用。
Nephrol Dial Transplant. 1996;11 Suppl 5:95-8. doi: 10.1093/ndt/11.supp5.95.
4
Effects of fructose ingestion on sorbitol and fructose 3-phosphate contents of erythrocytes from healthy men.摄入果糖对健康男性红细胞中山梨醇和果糖3 - 磷酸含量的影响。
Acta Diabetol. 1996 Jul;33(2):100-2. doi: 10.1007/BF00569417.
5
The aldose reductase inhibitor epalrestat exerts nephritic protection on diabetic nephropathy in db/db mice through metabolic modulation.醛糖还原酶抑制剂依帕司他通过代谢调节对 db/db 小鼠糖尿病肾病发挥肾脏保护作用。
Acta Pharmacol Sin. 2019 Jan;40(1):86-97. doi: 10.1038/s41401-018-0043-5. Epub 2018 Jun 21.
6
Erythrocyte sorbitol level as a predictor of the efficacy of epalrestat treatment for diabetic peripheral polyneuropathy.红细胞山梨醇水平作为依帕司他治疗糖尿病性周围神经病变疗效的预测指标。
J Diabetes Complications. 2006 Nov-Dec;20(6):367-70. doi: 10.1016/j.jdiacomp.2005.09.002.
7
Changes in erythrocyte sorbitol concentrations measured using an improved assay system in patients with diabetic complications and treated with aldose reductase inhibitor.采用改良检测系统测定糖尿病并发症患者经醛糖还原酶抑制剂治疗后红细胞山梨醇浓度的变化。
Diabetes Care. 1998 Apr;21(4):672-3. doi: 10.2337/diacare.21.4.672.
8
Fidarestat (SNK-860), a potent aldose reductase inhibitor, normalizes the elevated sorbitol accumulation in erythrocytes of diabetic patients.非达司他(SNK - 860),一种有效的醛糖还原酶抑制剂,可使糖尿病患者红细胞中升高的山梨醇积累恢复正常。
J Diabetes Complications. 2002 Mar-Apr;16(2):133-8. doi: 10.1016/s1056-8727(01)00175-1.
9
Aldose reductase inhibitor, epalrestat, reduces lipid hydroperoxides in type 2 diabetes.醛糖还原酶抑制剂依帕司他可降低2型糖尿病患者体内的脂质氢过氧化物水平。
Endocr J. 2009;56(1):149-56. doi: 10.1507/endocrj.k08e-237. Epub 2008 Nov 8.
10
Pharmacological properties of fidarestat, a potent aldose reductase inhibitor, clarified by using sorbitol in human and rat erythrocytes.通过在人和大鼠红细胞中使用山梨醇阐明强效醛糖还原酶抑制剂非达司他的药理特性。
Pharmacology. 2001 May;62(4):193-9. doi: 10.1159/000056094.

引用本文的文献

1
The Synergistic Effects of Polyol Pathway-Induced Oxidative and Osmotic Stress in the Aetiology of Diabetic Cataracts.多元醇途径诱导的氧化应激和渗透应激在糖尿病性白内障发病机制中的协同作用。
Int J Mol Sci. 2024 Aug 20;25(16):9042. doi: 10.3390/ijms25169042.
2
Formation of Fructose-Mediated Advanced Glycation End Products and Their Roles in Metabolic and Inflammatory Diseases.果糖介导的晚期糖基化终产物的形成及其在代谢和炎症性疾病中的作用。
Adv Nutr. 2017 Jan 17;8(1):54-62. doi: 10.3945/an.116.013912. Print 2017 Jan.
3
Prevention of non-enzymatic glycosylation (glycation): Implication in the treatment of diabetic complication.
非酶糖基化(糖基化)的预防:对糖尿病并发症治疗的意义。
Int J Health Sci (Qassim). 2016 Apr;10(2):261-77.