Evaluation of Metabolic State in Striatal Rat Model of Parkinson's Disease: before and after Deep Brain Stimulation
|Joana Guimarães1,2,5*, Eduardo Moura3,5, Elisabete Silva4,5, Carolina Garrett1,2,5, Maria Augusta Vieira-Coelho3,5
|1Neurology Department, Hospital de São João, Portugal
|2Neurology and Neurosurgery Unit of Clinical Neurosciences and Mental Health Department, Faculty of Medicine, University of Porto, Portugal
|3Pharmacology and Therapeutics Department, Faculty of Medicine, University of Porto, Portugal
|4Experimental Biology Department, Faculty of Medicine, University of Porto, Portugal
|5Institute for Molecular and Cell Biology, University of Porto, Portugal
|Corresponding Author :
Hospital de São João, Porto, Portugal
Tel: +351 22 5505640
|Received October 21, 2013; Accepted January 22, 2014; Published January 24, 2014
|Citation: Guimarães J, Moura E, Silva E, Garrett C, Vieira-Coelho MA (2014) Evaluation of Metabolic State in Striatal Rat Model of Parkinson’s Disease: before and after Deep Brain Stimulation. J Obes Weight Loss Ther 4:205. doi:10.4172/2165-7904.1000205
|Copyright: ©2014 Guimarães J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Weight loss occurs during the natural history of Parkinson’s disease (PD). This non-motor manifestation of the disease is reversed by deep brain stimulation of the sub thalamic nucleus (DBS-STN) therapeutics which is often associated with weight gain. Although it has been proposed that PD is associated with alterations in central energy metabolism the mechanisms responsible for this weight variation remain unknown. This study evaluates the weight profile and nutritional state of the 6-hydroxydopamine (6-OHDA) rat model of PD subjected to DBS-STN. Rats were rendered parkinsonian by bilateral injections of 6-OHDA into the striatum and electrodes were implanted bilaterally at the level of the STN. Rats were placed in metabolic cages for evaluation of weight, food and liquid intake and urine and fecal volume before and 2 and 4 weeks after the beginning of stimulation. Before stimulation began (2 weeks after 6-OHDA lesion), weight and metabolic parameters were similar between parkinsonian rats with and without electrodes and matched control rats. Two weeks after stimulation began (4 weeks after 6-OHDA lesion) and at the end of the study, 4 weeks after stimulation began (6 weeks after 6-OHDA lesion), body weight and the metabolic parameters evaluated remained unaltered between animal groups. Furthermore, at the end of the study, no statistically significant differences were found in efficiency of eating (change in weight/amount of food eaten) or weight gain between groups. In conclusion, in the rat model of PD with striatal dopaminergic neurodegeneration neither induction of PD or DBS-STN influenced weight variation or metabolic state. Additional mechanisms may be required to induce the altered metabolic state observed in PD patients before and after STN-DBS.