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,
neuroinflammation, abnormal aggregation of
protein, mitochondrial dysfunction, and decreased
dopamine, and finally result in energy supply insufficiency,
neurotransmitter dysregulation, aggregation and phosphorylation of α-
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.