Type 2 diabetes mellitus augments Parkinson's disease risk or the other way around: Facts, challenges and future possibilities.
Study Goal
The researchers aimed to review the literature on the relationship between high-fat diet, insulin resistance, and their potential role in augmenting Parkinson's disease risk.
Results Summary
The abstract suggests that high-fat diet and insulin resistance may contribute to Parkinson's disease by affecting sugar metabolism, oxidative stress, α-synuclein aggregation, inflammation, and mitochondrial function, though some studies contradict this link.
Population
General adult population, with specific focus on individuals with type 2 diabetes mellitus and those over 60 years of age.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
type 2 diabetes mellitus | increase | PD risk | adult population | - | augments | #1 |
hyperglycemia | increase | Parkinsonian feature | case controls possessing T2DM | - | corroborates the role | #2 |
insulin resistance | increase | PD risk | - | - | increased | #3 |
high fat diet | increase | sugar metabolism, oxidative stress, α-synuclein aggregation and accumulation, inflammatory response and mitochondrial function | PD models and sporadic PD | - | further connect | #4 |
anti-diabetic drugs | decrease | Parkinsonian symptoms | - | - | ameliorative effect | #5 |
anti-PD medications | no change | - | T2DM patients | - | vague outcome | #6 |
About 10% of the adult population is living with type 2 diabetes mellitus (T2DM) and 1% of the population over 60 years of age is suffering from Parkinson's disease (PD). A school of thought firmly believes that T2DM, an age-related disease, augments PD risk. Such relationship is reflected from the severity of PD symptoms in drug naive subjects possessing T2DM. Onset of Parkinsonian feature in case controls possessing T2DM corroborates the role of hyperglycemia in PD. A few cohort, meta-analysis and animal studies have shown an increased PD risk owing to insulin resistance. High fat diet and role of insulin signaling in the regulation of sugar metabolism, oxidative stress, α-synuclein aggregation and accumulation, inflammatory response and mitochondrial function in PD models and sporadic PD further connect the two. Although little is reported about the implication of PD in hyperglycemia and T2DM, a few studies have also contradicted. Ameliorative effect of anti-diabetic drugs on Parkinsonian symptoms and vague outcome of anti-PD medications in T2DM patients also suggest a link. The article reviews the literature supporting augmented risk of one by the other, analysis of proof of the concept, facts, challenges, future possibilities and standpoint on the subject.