Key result
GH treatment for 4 months significantly increased GHRtr mRNA in adipose tissue, increased GHR and decreased GHRtr mRNA in skeletal muscle, and decreased circulating GHBP.
Why the study?
Does GH substitution therapy alter the gene expression of GHR and GHRtr in adipose tissue and skeletal muscle in GH-deficient adults?
Does GH substitution therapy alter the gene expression of GHR and GHRtr in adipose tissue and skeletal muscle in GH-deficient adults?
GH treatment in GH-deficient adults differentially alters the mRNA expression of full-length and truncated GH receptors in adipose tissue and skeletal muscle.
Answers are grounded in this paper and cite their sources.
Does not support changing GH substitution practice; hypothesis-generating for tissue-specific receptor regulation in GH deficiency.
In humans at least two GH receptors are significantly expressed. One is the full-length receptor (GHR); the other is a truncated form (GHRtr), that lacks most of the intracellular domain. This receptor may inhibit the action of the full-length receptor. Circulating GH-binding protein (GHBP) is a proteolytically cleaved product from both of these receptors. The clinical relevance of the different receptor types is unknown. We examined the gene expression of GHR and GHRtr in human adipose tissue and skeletal muscle and the influence of GH treatment on this expression. Furthermore, we studied the relationship of circulating GHBP and body composition to GHR and GHRtr gene expression. Eleven adult GH-deficient patients were studied before and after 4 months of GH substitution therapy. Abdominal fat obtained by liposuction and femoral muscle biopsies were taken at baseline and after 4 months. Gene expression of GHR and GHRtr in adipose tissue and skeletal muscle was determined and expressed relative to the expression of beta-actin. Gene expression of GHR in abdominal sc adipose tissue was not altered, whereas the expression of GHRtr increased significantly. In skeletal muscle inverse changes were seen in the expression of messenger ribonucleic acid (mRNA) levels for the two GH receptor forms: expression of GHR increased significantly, whereas mRNA levels for GHRtr decreased. As expected, body composition changed with reduction of body fat mass after 4 months of GH treatment. Levels of circulating GHBP decreased significantly. We conclude that GH treatment in GH-deficient adults changes the expression of mRNA for GHR and GHRtr in adipose tissue and skeletal muscle. Whether these changes are responsible for the observed changes in body composition in response to GH treatment and the observed changes in levels of circulating GHBP, however, needs further elucidation.
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Fisker et al. (2001) studied Growth hormone (GH) deficiency (n=11). GH substitution therapy vs. Baseline (pre-treatment) was evaluated on Gene expression of GHR and GHRtr in adipose tissue and skeletal muscle. GH treatment for 4 months significantly increased GHRtr mRNA in adipose tissue, increased GHR and decreased GHRtr mRNA in skeletal muscle, and decreased circulating GHBP.
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