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
Article Information
Identifiers and Pagination:
Year: 2008Volume: 2
First Page: 29
Last Page: 36
Publisher Id: TONUTRJ-2-29
DOI: 10.2174/1874288200802010029
Article History:
Received Date: 11/03/2008Revision Received Date: 31/03/2008
Acceptance Date: 01/04/2008
Electronic publication date: 23/4/2008
Collection year: 2008
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.
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.