ECE2014 Poster Presentations Neuroendocrinology (27 abstracts)
1Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil, 2Department of Pharmacology, School of Medicine, State University of Campinas, Campinas, SP, Brazil.
In liver, melatonin (Mel) and glucocorticoids (GC) influence the systemic energy homeostasis. Animals without pineal gland present impairment in glycemic control, as in type-2 diabetes. In turn, Mel reduces the GC levels, particularly in nocturnal animals. We aimed to evaluate the influence of Mel, as well as GC receptor blockade by RU486 treatment on hepatic and pancreatic energy metabolism. Male Wistar rats were subjected to surgical removal of pineal and, 25 days after the surgery, treated with vehicle (PX) or RU486 (PX RU; 0.5 mg/100 g per 5 days). All the experiments were conducted at the end of the light phase of the light/dark cycle (ZT10). Animals were weighed and subjected to analysis of body composition by in vivo imaging system (FX PRO). Reduction of body weight (16%), muscle mass (41%) and adiposity (30%) was found in PX group, which was reversed by RU486 treatment. Circulating corticosterone were 30% higher in PX compared to control group (CTL, P≤0.05), despite the reduced glycemia (8%) and insulin levels (37%), both reversed by RU486 treatment. Additionally, PX increased in 28% the hepatic glycogen content, measured by digestion assay and histology (PAS). RT- PCR from liver tissue showed reduced mRNA to GCK (40%) in PX rats, compared to CTL (P≤0.05). PX RU showed increased mRNA to SREBP1c (10%), as well as decreased mRNA to PEPCK and G6Pase, compared to CTL (P≤0.05). The pancreatic islets were isolated from rats and incubated at four different glucose concentrations for measurement of insulin secreted (GSIS). Our results indicate increased insulin secretion in PX and PX RU in all concentrations analyzed. This finding corroborates overall results indicating that glucose intolerance in PX rats is characterized by hepatic insulin resistance and pancreatic insulin hyper secretion which can be a result of higher corticosterone levels.