Effects of astressin 2B and nesfatin-1 on food and water intake in Suncus murinus
Author(s)
Lu, Zengbing
Author(s)
Sakata, I.
Sakai, T.
Lin, G.
Rudd, J. A.
Date Issued
2019
Conference
NeuroGASTRO 2019
Abstract
Objective
Nesfatin-1 induces emesis and reduces feeding in Suncus murinus (house musk shrew). In the present studies, we examine if the action of nesfatin-1 to induce emesis and inhibit feeding can be prevented by the corticotropin-releasing factor receptor 2 (CRF2) antagonist, astressin 2B. Methods Shrews were anaesthetised with sodium pentobarbitone (40 mg/kg, i.p.) and then stereotaxically implanted with a guide cannula into the lateral ventricle. They were allowed 7-days recovery before being fasted overnight and administered astressin 2B (3 nmol, i.c.v.), or saline (5 μl i.c.v.), 15 minutes prior to nesfatin-1 (5 pmol, i.c.v.), or saline (5 μl, i.c.v.). Emesis and spontaneous behaviour were measured every h for 6 hours. Results Nesfatin-1 predictably reduced food intake, but it failed to emesis (P < 0.05, N = 6-8,). Surprisingly, astressin 2B alone also reduced food intake (P < 0.05, N = 6-8,). As a pretreatment, astressin 2B did not affect the action of nesfatin-1 to suppress feeding (P > 0.05, N = 6-8). Neither astressin 2B nor nesfatin-1 affected water consumption during the 6 hours assessment period. Conclusions Nesfatin-1 can inhibit food intake in the absence of emesis. The action of astressin 2B suggests that CRF2 is involved in mechanisms of feeding control, but the pathway may be independent of nesfatin-1 receptor systems. The studies were fully supported by a grant from the Research Grants Council of the Hong Kong SAR, China (Project no. UGC/FDS11/M02/16).
Nesfatin-1 induces emesis and reduces feeding in Suncus murinus (house musk shrew). In the present studies, we examine if the action of nesfatin-1 to induce emesis and inhibit feeding can be prevented by the corticotropin-releasing factor receptor 2 (CRF2) antagonist, astressin 2B. Methods Shrews were anaesthetised with sodium pentobarbitone (40 mg/kg, i.p.) and then stereotaxically implanted with a guide cannula into the lateral ventricle. They were allowed 7-days recovery before being fasted overnight and administered astressin 2B (3 nmol, i.c.v.), or saline (5 μl i.c.v.), 15 minutes prior to nesfatin-1 (5 pmol, i.c.v.), or saline (5 μl, i.c.v.). Emesis and spontaneous behaviour were measured every h for 6 hours. Results Nesfatin-1 predictably reduced food intake, but it failed to emesis (P < 0.05, N = 6-8,). Surprisingly, astressin 2B alone also reduced food intake (P < 0.05, N = 6-8,). As a pretreatment, astressin 2B did not affect the action of nesfatin-1 to suppress feeding (P > 0.05, N = 6-8). Neither astressin 2B nor nesfatin-1 affected water consumption during the 6 hours assessment period. Conclusions Nesfatin-1 can inhibit food intake in the absence of emesis. The action of astressin 2B suggests that CRF2 is involved in mechanisms of feeding control, but the pathway may be independent of nesfatin-1 receptor systems. The studies were fully supported by a grant from the Research Grants Council of the Hong Kong SAR, China (Project no. UGC/FDS11/M02/16).
SFU Affiliated Publication
Yes
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