Oral Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2013

Neuropeptide Y, acting through the Y1 receptor, suppresses pulsatile growth hormone secretion following short-term fasting in the mouse (#85)

Lili Huang 1 , Frederik Steyn 1 , Hwee Yim Angeline Tan 1 , Johannes Veldhuis 2 , Herbert Herzog 3 , Chen Chen 1
  1. School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, 4072, Australia
  2. Department of Medicine, Endocrine Research Unit, Mayo School of Graduate Medical Education, Clinical Translational Science Center, Mayo Clinic, , Rochester, MN 55905, USA
  3. Neuroscience Division, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, Sydney, NSW 2010, Australia

The neuropeptide Y (NPY) system in the brain plays an important role in regulating food intake and energy expenditure. Increased hypothalamic NPY expression as shown in obese animal models coincides with a reduction in growth hormone (GH) secretion1,2  . Likewise, this inverse relationship also occurs during fasting in mice3 . Whether increased NPY contributes to the impairment of pulsatile GH secretion in the fasting mouse remains unknown.

Using NPY knockout mice, pulsatile GH secretion was characterized following 6 hours of food withdrawal. Furthermore, to determine whether NPY receptor mediates this process, GH secretion was assessed in Y1 (the dominant post-synaptic receptor in mediating food intake)4  and Y2 (the dominant pre-synaptic receptor that negatively regulates NPY release)5  receptor knockout mice.

Deletion of NPY maintained pulsatile GH secretion in mice following 6 hours of food withdrawal. This was characterized by a significant increase in total (223 ± 29.8 vs 47.0 ± 11.6ng/ml per 6h, p<0.001), pulsatile (207 ± 29.8 vs 42.6 ± 11.1ng/ml per 6h, p<0.001), and the mass of GH secreted per burst (70.7 ± 18.6 vs 10.0 ± 1.87ng/ml, p=0.002) compared with that in fasting control mice. The secretion of GH in fasted NPY knockout mice was comparable to that observed in mice under normal fed conditions. In addition, the recovery of GH secretion was observed in Y1 receptor but not Y2 receptor knockout mice.

Observations suggest NPY contributes to the suppression of GH secretion following short-term fasting in mice, a process mediated via the Y1 receptor. Data demonstrate the integration of neuronal mechanisms that modulate the release of GH to food intake. Extrapolation of observations provides essential information to define mechanisms that regulate anabolic GH profiles under positive or negative energy conditions.

This work was supported by NHMRC and The University of Queensland. L. Huang receives postgraduate scholarships from China (CSC) and The University of Queensland.
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