Abstract
We hypothesize that glucosensor mechanisms other than that mediated by glucokinase (GK) operate in hypothalamus and hindbrain of the carnivorous fish species rainbow trout and stress affected them. Therefore, we evaluated in these areas changes in parameters which could be related to putative glucosensor mechanisms based on liver X receptor (LXR), mitochondrial activity, sweet taste receptor, and sodium/glucose co-transporter 1 (SGLT-1) 6h after intraperitoneal injection of 5 mL.Kg-1 of saline solution alone (normoglycaemic treatment) or containing insulin (hypoglycaemic treatment, 4 mg bovine insulin.Kg-1 body mass), or D-glucose (hyperglycaemic treatment, 500 mg.Kg-1 body mass). Half of tanks were kept at a 10 Kg fish mass.m-3 and denoted as fish under normal stocking density (NSD) whereas the remaining tanks were kept at a stressful high stocking density (70 kg fish mass.m-3) denoted as HSD. The results obtained in non-stressed rainbow trout provide evidence, for the first time in fish, that manipulation of glucose levels induce changes in parameters which could be related to putative glucosensor systems based on LXR, mitochondrial activity and sweet taste receptor in hypothalamus, and a system based on SGLT-1 in hindbrain. Stress altered the response of parameters related to these systems to changes in glycaemia.
Highlights
Glucosensor mechanisms allow vertebrates to monitor changes in glucose levels at different central or peripheral locations [1]
We have demonstrated the presence in brain areas of a carnivorous fish species like rainbow trout (Oncorhynchus mykiss) of a glucosensor mechanism based on GK-glucose facilitative transporter type 2 (GLUT2)-KATP similar to that characterized in mammalian GE neurons and pancreatic β-cells, which is related to the control of food intake, and to counterregulatory mechanisms [1,13,14,15]
We evaluated changes in parameters related to GK-mediated glucosensing, such as GK and pyruvate kinase (PK) activities, and mRNA abundance of GK, GLUT2, PK, 6-phosphofructo 1-kinase (PFK), inward rectifier K+ channel pore type 6.x-like (Kir6.x-like), and sulfonylurea receptor-like (SUR-like), as well as in the mRNA abundance of neuropeptides related to the control of food intake, such as neuropeptide Y (NPY), pro-opio melanocortin A1 (POMC-A1), cocaine and amphetamine-related transcript (CART), agouti-related peptide (AgRP), and cortocotropin releasing factor (CRF)
Summary
Glucosensor mechanisms allow vertebrates to monitor changes in glucose levels at different central or peripheral locations [1]. Glucosensing in brain areas like hypothalamus and hindbrain has been related to the control of food intake as well as to counter-regulatory mechanisms to restore plasma levels of metabolites [1]. The mechanisms involved in glucosensing have been partially elucidated in mammals [1,2]. The most important and best characterized mechanism is that demonstrated in pancreatic β-cells and glucose-excited (GE) neurons. Glucosensors in Trout Brain and analysis, decision to publish, or preparation of the manuscript
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