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健康与特定神经退行性疾病中的人类葡萄糖转运蛋白

Human Glucose Transporters in Health and Selected Neurodegenerative Diseases.

作者信息

Szablewski Leszek

机构信息

Chair and Department of General Biology and Parasitology, Medical University of Warsaw, Chałubińskiego Str. 5, 02-004 Warsaw, Poland.

出版信息

Int J Mol Sci. 2025 Jul 31;26(15):7392. doi: 10.3390/ijms26157392.


DOI:10.3390/ijms26157392
PMID:40806521
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12347752/
Abstract

Glucose is the main source of energy and the source of carbon for the biosynthesis of several molecules, such as neurotransmitters, for most mammalian cells. Therefore, the transport of glucose into cells is very important. There are described three distinct families of glucose transporters: facilitative glucose transporters (GLUTs), sodium-dependent glucose cotransporters (SGLTs), and a uniporter, the SWEET protein. Impaired function and/or expression of these transporters due to, for example, mutations in their genes, may cause severe diseases. Associations with the impaired function of glucose transporters have been described in the case of neurodegenerative diseases (NDs) such as Alzheimer's disease, Parkinson's disease, Huntington's disease, GLUT1-deficiency syndrome, stroke, and traumatic brain injury. Changes in the presence of glucose transporters may be a cause of NDs, and they may be the effect of NDs. On the other hand, in many cases of neurodegenerative diseases, changes in the expression of glucose transporters may be a targeted therapy in the treatment of patients with these diseases.

摘要

对于大多数哺乳动物细胞而言,葡萄糖是主要的能量来源以及多种分子(如神经递质)生物合成的碳源。因此,葡萄糖进入细胞的转运过程非常重要。目前已描述了三类不同的葡萄糖转运蛋白家族:易化葡萄糖转运蛋白(GLUTs)、钠依赖性葡萄糖共转运蛋白(SGLTs)以及一种单向转运体——SWEET蛋白。例如,由于其基因发生突变导致这些转运蛋白的功能和/或表达受损,可能会引发严重疾病。在神经退行性疾病(NDs)如阿尔茨海默病、帕金森病、亨廷顿病、GLUT1缺乏综合征、中风和创伤性脑损伤的病例中,已描述了与葡萄糖转运蛋白功能受损的关联。葡萄糖转运蛋白存在情况的变化可能是神经退行性疾病的一个病因,也可能是神经退行性疾病的一个结果。另一方面,在许多神经退行性疾病病例中,葡萄糖转运蛋白表达的变化可能是治疗这些疾病患者的一种靶向疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cef/12347752/f5811b926da1/ijms-26-07392-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cef/12347752/d70449c9bbdb/ijms-26-07392-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cef/12347752/f5811b926da1/ijms-26-07392-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cef/12347752/d70449c9bbdb/ijms-26-07392-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cef/12347752/f5811b926da1/ijms-26-07392-g002.jpg

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本文引用的文献

[1]
Parkinson's disease and glucose metabolism impairment.

Transl Neurodegener. 2025-2-17

[2]
Associations Between Diabetes Mellitus and Neurodegenerative Diseases.

Int J Mol Sci. 2025-1-10

[3]
Metabolic Dysfunction in Parkinson's Disease: Unraveling the Glucose-Lipid Connection.

Biomedicines. 2024-12-13

[4]
Targeting Glucose Metabolism: A Novel Therapeutic Approach for Parkinson's Disease.

Cells. 2024-11-13

[5]
Metabolic dysregulation in Huntington's disease: Neuronal and glial perspectives.

Neurobiol Dis. 2024-10-15

[6]
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JCI Insight. 2024-10-22

[7]
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Annu Rev Physiol. 2024-2-12

[8]
A reversible state of hypometabolism in a human cellular model of sporadic Parkinson's disease.

Nat Commun. 2023-11-23

[9]
Glucose metabolism impairment in Parkinson's disease.

Brain Res Bull. 2023-7

[10]
Exendin-4 and linagliptin attenuate neuroinflammation in a mouse model of Parkinson's disease.

Neural Regen Res. 2023-8

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