Abstract
There is a mutual relationship between metabolic and neurodegenerative diseases. However, the causal relationship in this crosstalk is unclear and whether Parkinson’s disease (PD) causes a posterior impact on metabolism remains unknown. Considering that, this study aimed to evaluate the appearance of possible changes in metabolic homeostasis due to 6-hydroxydopamine (6-OHDA) administration, a neurotoxin that damage dopaminergic neurons leading to motor impairments that resemble the ones observed in PD. For this, male Wistar rats received bilateral 6-OHDA administration in the dorsolateral striatum, and the motor and metabolic outcomes were assessed at 7, 21, or 35 days post-surgical procedure. Dexamethasone, a diabetogenic glucocorticoid (GC), was intraperitoneally administered in the last 6 days to challenge the metabolism and reveal possible metabolic vulnerabilities caused by 6-OHDA. Controls received only vehicles. The 6-OHDA-treated rats displayed a significant decrease in locomotor activity, exploratory behavior, and motor coordination 7 and 35 days after neurotoxin administration. These motor impairments paralleled with no significant alteration in body mass, food intake, glucose tolerance, insulin sensitivity, and biochemical parameters (plasma insulin, triacylglycerol, and total cholesterol levels) until the end of the experimental protocol on days 35–38 post-6-OHDA administration. Moreover, hepatic glycogen and fat content, as well as the endocrine pancreas mass, were not altered in rats treated with 6-OHDA at the day of euthanasia (38th day after neurotoxin administration). None of the diabetogenic effects caused by dexamethasone were exacerbated in rats previously treated with 6-OHDA. Thus, we conclude that bilateral 6-OHDA administration in the striatum causes motor deficits in rats with no impact on glucose and lipid homeostasis and does not exacerbate the adverse effects caused by excess GC. These observations indicate that neurodegeneration of dopaminergic circuits in the 6-OHDA rats does not affect the metabolic outcomes.
Highlights
The first description of Parkinson’s disease (PD) was made by James Parkinson in the early nineteenth century (Pearce, 1989)
There were no significant differences in the number of central crosses as well as in the number of rearing behavior in both 6-OHDA and 6-OHDA + Dexamethasone group (Dexa) groups compared to their respective Control groups (Figures 3C,D,G,H)
Central Administration of 6-OHDA Did Not Affect Plasma Insulin, Triacylglycerol, and Total Cholesterol Levels To verify whether motor impairment caused by bilateral 6-OHDA administration could be associated with alteration in peripheral glucose and lipid metabolism, we evaluated the insulinemia and some circulating lipid levels
Summary
The first description of Parkinson’s disease (PD) was made by James Parkinson in the early nineteenth century (Pearce, 1989). The disease is characterized by a slow and progressive loss of dopaminergic neurons from the substantia nigra resulting in a gradual loss of motor functions (Stern et al, 2012). Approximately 40% of the dopaminergic neurons are intact and the presence of dopamine in the striatum is restricted to approximately 20–30% of the normal condition (Riederer and Wuketich, 1976). Epidemiological studies associate the etiology with several risk factors such as neuronal aging, genetic and environmental factors, viruses and inadequate eating habits (Marttila et al, 1977; Gorell et al, 1997; Mattson, 2003; Steenland et al, 2006; Goldman, 2010)
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