High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress.
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2020
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Obesity is a health problem that has been associated with neuroinflammation, decreased cognitive
functions and development of neurodegenerative diseases. Parkinson’s disease (PD) is a chronic
neurodegenerative condition characterized by motor and non-motor abnormalities, increased
brain inflammation, α-synuclein protein aggregation and dopaminergic neuron loss that is
associated with decreased levels of tyrosine hydroxylase (TH) in the brain. Diet-induced obesity
is a global epidemic and its role as a risk factor for PD is not clear. Herein, we showed that 25
weeks on a high-fat diet (HFD) promotes significant alterations in the nigrostriatal axis of Wistar
rats. Obesity induced by HFD exposure caused a reduction in TH levels and increased TH
phosphorylation at serine 40 in the ventral tegmental area. These effects were associated with
insulin resistance, increased tumor necrosis factor-α levels, oxidative stress, astrogliosis and
microglia activation. No difference was detected in the levels of α-synuclein. Obesity also
induced impairment of locomotor activity, total mobility and anxiety-related behaviors that
were identified in the open-field and light/dark tasks. There were no changes in motor
coordination or memory. Together, these data suggest that the reduction of TH levels in the
nigrostriatal axis occurs through an α-synuclein-independent pathway and can be attributed to
brain inflammation, oxidative/nitrosative stress and metabolic disorders induced by obesity.
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Parkinson’s disease, Inflammation, Locomotion, Anxiety
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BITTENCOURT, A. et al. High fat diet-induced obesity causes a reduction in brain tyrosine hydroxylase levels and non-motor features in rats through metabolic dysfunction, neuroinflammation and oxidative stress. Nutritional Neuroscience, 2020. Disponível em: <https://www.tandfonline.com/doi/full/10.1080/1028415X.2020.1831261>. Acesso em: 11 out. 2022.