Parkinson’s Disease and Diabetes Mellitus: Synergistic Effects on Pathophysiology and GI Motility

Purpose of Review: Parkinson’s disease and diabetes affect an increasing proportion of the aging global population. Both conditions extensively affect gastrointestinal (GI) motility with similar and differing clinical symptoms. Nonetheless, GI symptoms in Parkinson’s disease and diabetes pose significant morbidity and impairment of quality of life. Their pathophysiology is poorly understood, and therefore, effective treatment options are lacking. Recent Findings: Parkinson’s disease patients have oropharyngeal dysphagia and constipation. They also have mild or absent upper GI symptoms associated with delayed gastric emptying, which is prevalent in 70% of patients. Delayed gastric emptying in Parkinson’s disease leads to erratic medication absorption and fluctuating motor symptoms. Half of diabetics have upper GI symptoms, which correlate to gastric emptying and changes in brain activity of the insular cortex. The majority of diabetics also have constipation. Diabetics have an increased risk for developing Parkinson’s disease and anti-diabetic medications are associated with risk reduction of developing Parkinson’s disease. Hyperglycemia is associated with advanced glycated end products formation and acceleration of α-synuclein aggregation. GLP-1 receptor agonists have also demonstrated efficacy in improving motor symptoms and cognition in Parkinson’s disease patients with diabetes. Summary: Parkinson’s disease and diabetes are pan-enteric disorders with significant GI symptoms and impairment of gut motility. Both conditions have synergistic pathophysiologies that propagate neurodegenerative changes. Treatment options for GI symptoms in diabetic and Parkinson’s disease patients are lacking. Anti-diabetic treatment improves motor symptoms in Parkinson’s disease, however, its effect on GI symptoms is unclear.