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• W3081617008 abstract "Abstract To explore the possible mechanism of weight loss in Parkinson's disease (PD). Bilateral injections of 6‐hydroxydopamine (6‐OHDA) into substantia nigra (SN) were performed to induce the PD model rats. The rotarod test, food intake, body weight, and interscapular brown adipose tissue (IBAT) weight were recorded 6 weeks postoperation. HE staining was performed to observe the morphology of multilocular adipose cells in IBAT. Immunohistochemistry and western blot were used to determine the protein levels of tyrosine hydroxylase (TH) in the SN, and the levels of uncoupling protein 1 (UCP1), peroxisome proliferator‐activated receptor gamma coactivator‐1α (PGC‐1α), phosphorylated‐hormone sensitive lipase (p‐HSL), HSL, TH, β3‐adrenergic receptor (β3‐AR), cyclic adenosine monophosphate (cAMP), and protein kinase A (PKA) in IBAT. After treatment with 6‐OHDA for 6 weeks, 6‐OHDA rats exhibited decreased TH expression in SN accompanied with shortened staying time on the rotating rod. This motor impairment paralleled with no significant alteration in body mass, IBAT weight, and food intake until the end of the experimental protocol. However, the decreasing diameter of the single fat vesicle in IBAT was observed in the 6‐OHDA group. Meanwhile, compared with the control group, the protein expression of UCP1, PGC‐1α, p‐HSL, TH, β3‐AR, cAMP, and PKA in IBAT were increased significantly in the 6‐OHDA group, whereas no obvious change in the expression of HSL. The present study suggested an increased energy expenditure and activation of the β3‐AR‐cAMP‐PKA signaling pathway in the IBAT after the destruction of the dopamine system in the SN of the rat." @default.
• W3081617008 created "2020-09-08" @default.
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• W3081617008 date "2020-09-14" @default.
• W3081617008 modified "2023-09-23" @default.
• W3081617008 title "Increased energy expenditure and activated <scp>β3‐AR‐cAMP‐PKA</scp> signaling pathway in the interscapular brown adipose tissue of <scp>6‐OHDA</scp>‐induced Parkinson's disease model rats" @default.
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• W3081617008 doi "https://doi.org/10.1002/ar.24505" @default.
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