Ghrelin effects on central glucosensing and energy homeostasis-related peptides in rainbow trout

Although the role of ghrelin (GHRL) on fish appetite regulation had been widely studied in past years, its involvement in the regulation of glucose metabolism had been little explored. In the present study we hypothesize that GHRL may have a role in the regulation of glucose homeostasis in fish. Therefore, we carried out different experimental approaches in rainbow trout to assess brain glucosensing potential and glucose metabolism in response to GHRL treatment. We found that after either systemic or central GHRL administration to trout deprived of food, glycemia remained unaffected, whereas (in clear contrast with the mammalian model) a consistent activation of the main glucosensing markers (glucose transporter 2, glucokinase, and ATP-sensitive inward rectified K+ channel) was noticed in both hypothalamus and hindbrain. Some of these results were further confirmed by in vitro incubations of hypothalamus and hindbrain in the presence of GHRL. Despite the lack of changes in glycemia, we suggest that the changes elicited by GHRL on the glucosensing system are direct and could be related to a helper action of this hormone when glucose arrived in the postprandial phase. Moreover, we also studied the effect of GHRL treatment on the expression of several food intake-related neuropeptides, such as neuropeptide Y, cocaine- and amphetamine-regulated transcript, pro-opiomelanocortin, and corticotropin-releasing factor. We observed an important variability in the effects of GHRL attributable either to the route of GHRL administration or to the brain regions assessed, which could help explain the contradictory results described in fish literature about GHRL role in food intake control.