Glucose metabolism impairment in Parkinson's disease

被引：45

作者：

Dai, Chengcheng ^{[1
]}

Tan, Changhong ^{[1
]}

Zhao, Lili ^{[1
]}

Liang, Yi ^{[1
]}

Liu, Guohui ^{[1
]}

Liu, Hang ^{[1
]}

Zhong, Yuke ^{[1
]}

Liu, Zhihui ^{[1
]}

Mo, Lijuan ^{[1
]}

Liu, Xi ^{[1
,2
]}

Chen, Lifen ^{[1
,2
]}

机构：

[1] Chongqing Med Univ, Affiliated Hosp 2, Dept Neurol, 74 Linjiang Rd, Chongqing 400010, Peoples R China

[2] 74 Linjiang Rd, Chongqing 400010, Peoples R China

来源：

BRAIN RESEARCH BULLETIN | 2023年 / 199卷

基金：

中国国家自然科学基金;

关键词：

Parkinson's disease; Glucose metabolism impairment; Pathophysiological mechanism; Energy supply insufficiency; Therapy; MITOCHONDRIAL COMPLEX-I; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GAPDH; BRAIN-BARRIER PERMEABILITY; GLYCATION END-PRODUCTS; MPTP MOUSE MODEL; ALPHA-SYNUCLEIN; INSULIN-RESISTANCE; OXIDATIVE STRESS; SUBTHALAMIC NUCLEUS; DIABETES-MELLITUS;

D O I：

10.1016/j.brainresbull.2023.110672

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Impairments in systematic and regional glucose metabolism exist in patients with Parkinson's disease (PD) at every stage of the disease course, and such impairments are associated with the incidence, progression, and special phenotypes of PD, which affect each physiological process of glucose metabolism including glucose uptake, glycolysis, tricarboxylic acid cycle, oxidative phosphorylation, and pentose phosphate shunt pathway. These impairments may be attributed to various mechanisms, such as insulin resistance, oxidative stress, abnormal glycated modification, blood-brain-barrier dysfunction, and hyperglycemia-induced damages. These mechanisms could subsequently cause excessive methylglyoxal and reactive oxygen species production, neuro-inflammation, abnormal aggregation of protein, mitochondrial dysfunction, and decreased dopamine, and finally result in energy supply insufficiency, neurotransmitter dysregulation, aggregation and phosphorylation of alpha-synuclein, and dopaminergic neuron loss. This review discusses the glucose metabolism impairment in PD and its pathophysiological mechanisms, and briefly summarized the currently-available therapies targeting glucose metabolism impairment in PD, including glucagon-likepeptide-1 (GLP-1) receptor agonists and dual GLP-1/ gastric inhibitory peptide receptor agonists, metformin, and thiazoledinediones.

引用

页数：12

共 204 条

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