Key result
The GHR allelic variant lacking exon 3 was not associated with significant differences in overnight mean GH secretion (6.2 vs 6.8 ng/ml) or insulin sensitivity in prepubertal low birth weight children.
Why the study?
Does the GHR allelic variant affect nocturnal GH concentrations, IGF-I/IGFBP-3 levels, or insulin sensitivity in prepubertal LBW children?
Observational (n=38)
Does the GHR allelic variant affect nocturnal GH concentrations, IGF-I/IGFBP-3 levels, or insulin sensitivity in prepubertal LBW children?
Absolute Event Rate: 6.2% vs 6.8%
The GHR allelic variant does not appear to play a significant role in regulating the GH-IGF-I/BP3 axis or insulin sensitivity in prepubertal low birth weight children.
No association found in this cohort; leaves open any role for GHR exon 3 variant in other LBW populations or developmental stages.
Growth hormone may help to increase final height in patients with short stature, but its efficacy is variable. It has been recently reported that the isoform of the GH receptor (GHR) that lacks exon 3 (d3-GHR) is associated with a greater growth response to GH therapy. We hypothesized that nocturnal growth hormone concentrations, basal IGF-I and IGFBP-3 levels, and insulin sensitivity might show variations among individuals depending on their GHR allelic variant. To test this hypothesis, we studied 38 prepubertal LBW children with nocturnal GH concentrations, IGF-I and IGFBP-3 levels and insulin sensitivity during OGTT and Insulin test. The GHR allelic variant was analyzed through multiplex PCR analysis in DNA from peripheral leukocytes. Characteristics of the overnight GH secretion [(mean GH: 6.8 +/- 0.6 vs. 6.2 +/- 0.5 ng/ml), (AUC: 3,227 +/- 280 vs. 2,908 +/- 212 ng/ml.min), (peak number: 4.4 +/- 0.3 vs. 4.4 +/- 0.2), (amplitude: 12 +/- 1.1 vs. 10.8 +/- 1.1 ng/ml)] did not differ between groups (f1/f1 vs. f1/d3 plus d3/d3). In addition, we did not observe any significant differences in serum IGF-I SDS (-0.49 +/- 0.26 vs. -0.40 +/- 0.35) or IGFBP-3 SDS (-1.21 +/- 0.24 vs. -0.89 +/- 0.21) nor in insulin sensitivity (WIBSI: 12 +/- 1.2 vs. 10.8 +/- 1.1) in LBW children with full length GHR compared to children carrying at least one GHRd3 allele. The distribution of the f1/f1 allelic variant and fi/d3 or d3/d3 was similar in the LBW children with or without catch-up growth. These results suggest that the GHR allelic variant does not play a significant role in the regulation of GH-IGF-I/BP3 axis or in insulin sensitivity in prepubertal LBW children.
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Mericq et al. (2007) conducted an observational in Small for Gestational Age / Low Birth Weight (n=38). GHR allelic variant lacking exon 3 (f1/d3 or d3/d3) vs. Full length GHR (f1/f1) was evaluated on Overnight mean GH secretion (ng/ml). The GHR allelic variant lacking exon 3 was not associated with significant differences in overnight mean GH secretion (6.2 vs 6.8 ng/ml) or insulin sensitivity in prepubertal low birth weight children.
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