We previously obtained evidence in rainbow trout for the presence and response to changes in circulating levels of glucose (induced by intraperitoneal hypoglycaemic and hyperglycaemic treatments) of glucosensing mechanisms dependent on liver X receptor (LXR), production of reactive oxygen species (ROS) in mitochondria inducing enhanced expression of uncoupling protein 2 (UCP2), and sweet taste receptor in hypothalamus, and on sodium/glucose co-transporter 1 (SGLT-1) in hindbrain. However those effects of glucose might be indirect. Therefore, we evaluated in a first experiment in pools of hypothalamus and hindbrain incubated for 6h at 15 °C in modified Hanks' medium containing 2, 4, or 8 mM D-glucose the response of parameters related to these glucosensing mechanisms. The responses observed in some cases were consistent with glucosensing capacity. In a second experiment, pools of hypothalamus and hindbrain were incubated for 6h at 15 °C in modified Hanks' medium with 8 mM D-glucose alone (control) or containing 1 mM phloridzin (SGLT-1 antagonist), 20 μM genipin (UCP2 inhibitor), 1 μM trolox (ROS scavenger), 100 μM bezafibrate (T1R3 inhibitor), and 50 μM geranyl-geranyl pyrophosphate (LXR inhibitor). The response observed in the presence of these specific inhibitors/antagonists further supports that critical components of the different glucosensing mechanisms are functioning in rainbow trout hypothalamus and hindbrain.
- Received January 19, 2016.
- Accepted March 3, 2016.
- © 2016. Published by The Company of Biologists Ltd