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J Appl Physiol (September 11, 2008). doi:10.1152/japplphysiol.90772.2008
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Submitted on June 16, 2008
Revised on August 11, 2008
Accepted on September 4, 2008

Upper Airway Loading Induces Growth Retardation and Changes in Local Chondrocyte IGF-1 Expression is Reversed by Stimulation of GH Release in Juvenile Rats

Yael Segev1*, Nilly Berdugo-Boura1, Orit Porati1, and Ariel Tarasiuk2

1 Faculty of Health Sciences, Ben-Gurion University of the Negev
2 Soroka University Medical Center

* To whom correspondence should be addressed. E-mail: yaelse{at}bgu.ac.il.

Chronic airway loading (CAL) impairs growth in juvenile rats. The effects of CAL on epiphyseal growth plate (EGP) structure and insulin-like growth factor-1 (IGF-1) gene expression were not explored. Little is known about whether stimulants of endogenous growth hormone (GH) secretion can normalize this growth impairment. This study explored the effect of CAL on circulating and EGP GH/IGF-1 pathway GH and the effect of ritanserin (endogenous GH stimulant) on somatic growth and the GH/IGF-1 axis. We hypothesize that CAL will lead to a decrease in body temperature (Tb) and alterations of GH/IGF-1 pathways, consequently leading to growth retardation. The tracheae of 22-day-old male rats were obstructed by tracheal banding (38 sham controls, 42 CAL). Tibial EGP morphometry, liver and EGP IGF mRNA and serum GH and IGF-1 levels were analyzed using qPCR and ELISA. Tb and locomotion activity (MA) were measured with telemetric transmitters inserted into the abdominal cavity. CAL animals had lower Tb and MA despite preserved food consumption. CAL impairs both tibial and tail length gains. Tail and tibial length gains inversely correlated with tracheal resistance. Circulating GH and IGF-1, liver and EGP IGF-1 mRNA and EGP width were decreased in the CAL group. Ritanserin administration to CAL animals normalized circulating and local EGP GH and IGF-1 levels and minimized this longitudinal growth impairment. We conclude that CAL causes growth delay associated with alterations in the GH/IGF-1 axis. Stimulation of GH release by ritanserin restored both global and local GH/IGF-1 pathways, yet growth parameters were only partially restored.







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