Meeting Abstract
38.8 Tuesday, Jan. 5 The Effects of Acute Cortisol Administration on Appetite Control in the Tilapia JANZEN, WJ*; RILEY, LG; California State University, Fresno; California State University, Fresno whitneyjanzen@yahoo.com
In response to a stressor, an animal’s physiology is altered in an attempt to maintain homeostasis and efficiently utilize its limited metabolic energy. Cortisol, a stress hormone, has widespread actions which mediate the response to stress by coordinating a set of physiological changes allowing an animal to restore homeostasis after a stressor. There are few a reports describing a reduction in appetite in stressed in fish; however, how stress influences the endocrine control of appetite has yet to be elucidated. The objective of this study was to investigate the short-term effects of cortisol on the endocrine regulation of appetite in the tilapia (Oreochromis mossambicus). Fish were given a single intraperitoneal injection of cortisol at 2 µg/g BW (low dose), 10 µg/g BW (high dose), or vehicle only (control). Tissue and blood samples were collected at 24 and 48 h post-injection. Pre-pro mRNA levels of the ghrelin receptor (GRLN-R), as well as mRNA levels of each GRLN-R isoform (GHS-R1a and -1b), and neuropeptide Y (NPY) were measured from brain. Plasma ghrelin levels were also measured. Plasma ghrelin and ghrelin mRNA levels in the brain were significantly suppressed in fish injected with the low dose of cortisol. In addition, mRNA levels of NPY were significantly increased in animals receiving the low dose of cortisol. GHS-R1b mRNA levels were significantly elevated in brain, whereas no change in pre-pro GRLN-R or GHS-R1a mRNA was observed. Our data showed that cortisol inhibited ghrelin mRNA levels providing a possible mechanism for the reduction of food intake reported in fish during stress. However, NPY mRNA levels were significantly elevated following cortisol treatment suggesting that NPY may be playing other roles in regulating overall metabolism in fish. This work was supported by the NSF (IOS-0639771) awarded to LGR.
