RESEARCH ARTICLE


Hypothalamic Noradrenergic Hyperactivity and Detrimental Bone Status in an Animal Model of Nutritional Growth Retardation



María I. Olivera1, Gabriela E. Compagnucci1, Cecilia V. Compagnucci1, Christian E. Lezón1, Patricia Mandalunis2, Sandra I. Hope3, Liliana G. Bianciotti4, Juan C. Elverdin1, Rosa M. Alippi1, Marcelo S. Vatta3, Patricia M. Boyer*, 1
1 Department of Physiology, School of Dentistry, University of Buenos Aires, Argentina
2 Department of Histology and Embriology , School of Dentistry, University of Buenos Aires, Argentina
3 Department of Physiology (IQUIMEFA-CONICET), School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina
4 Department of Pathophysiology, School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina


© 2008 Olivera et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Physiology, School of Dentistry, University of Buenos Aires, Argentina; E-mail:pboyer@fisio.odon.uba.ar


Abstract

We have studied hypothalamic noradrenergic activity in relation with bone status in a nutritional growth retardation model (ND). Control rats (C) were fed ad libitum. ND received 80% of the diet consumed by C for 4 weeks and later refed ad libitum for 8 weeks. Food restriction induced detrimental effects on body and femur weight and length (P<0.05) and bone biomechanical properties (P<0.001). Thickness of proliferative and hypertrophic zone (µm) of growth plate cartilage and bone volume (%, mean±SE) were 225.96±5.70 v. 280.70±12.52, 95.16±5.81 v. 134.60±9.30, 17.64±3.23 v. 26.80±2.03, respectively (P<0.05); anterior and posterior hypothalamus norepinephrine uptake and release and tyrosine hydroxylase activity (% of control) were 79.05±3.56, 67.00±10.00, 164.26±16.58 and 80.65±5.92, 147.00±1.00, 152.42±9.30, respectively (P<0.05). Thus, impaired biomechanical bone performance in ND could be due, in part, to the increased hypothalamic noradrenergic activity in response to restriction. Normalization of parameters with refeeding suggests no long-term side-effects in undernourished rats.

Keywords: Nutritional growth retardation, bone status, hypothalamic noradrenergic activity.