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Submitted on May 4, 2006
Accepted on October 2, 2006
Section of Endocrinology and Metabolism Department of Medicine, University of Illinois at Chicago, Chicago Illinois; Research and Development Division, Jesse Brown VA Medical Center, Chicago Illinois; Department of Pharmacology and Institute for Basic Medical Science, Kyunghee University School of Medicine, Seoul, Korea
* To whom correspondence should be addressed. E-mail: Kineman{at}uic.edu.
To determine if the severity of the catabolic conditions differentially regulates the GH-axis, male mice were either fed ad libitum or fasted for 12, 24 and 48 h. Hypothalami, pituitaries and stomachs were collected for assessment of mRNA levels by quantitative real-time RT-PCR, and blood collected for measurement of plasma hormone and metabolite levels by commercial assay kits. Overnight (12 h) fasting resulted in a significant suppression of circulating glucose, insulin, IGF-I and leptin levels and an increase in corticosterone, FFAs and n-octanoyl ghrelin levels and these directional changes were maintained at the 24 h and 48 h time points. Fasting (24 h) also increased circulating GH levels, which was associated with an increase in pituitary mRNA levels for GHRH receptor (GHRH-R) and ghrelin receptor (GHS-R) and a decrease in mRNA levels for somatostatin (SST) receptor subtypes, SSTR2, SSTR3 and SSTR5, where the changes in GHS-R and SSTR expression persisted after 48 h of fasting. Hypothalamic SST mRNA levels were not altered by fasting, while there was a transient rise in stomach SST mRNA levels 24 h after food withdrawal. In contrast, there was a biphasic effect of fasting on GHRH expression. GHRH mRNA levels were significantly elevated at 12 and 24 h, but fell to 
50% of fed controls 48 h after food withdrawal. A sequential rise in hypothalamic NPY and CRH mRNA levels preceded the fall in GHRH expression, where fasting-induced changes in CRH and GHRH mRNA levels were not observed in 48 h-fasted NPY knockout mice. These observations, in light of previous reports showing both NPY and CRH can inhibit GHRH expression and GH release, suggest that these neuronal systems may work in concert to control the ultimate impact of fasting on GH-axis function.
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