March 05, 2015
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Summer daylight exposure linked to growth in GH-deficient children

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SAN DIEGO — Genes modulating growth and summer daylight exposure are subject to a complex gene–environment interaction in response to recombinant human growth hormone, according to research presented here.  

Researchers said a possible linking mechanism is the biological regulation of the circadian clock.

Peter Clayton, MD, PhD, MRCP, FRCC, BSc, of the University of Manchester, United Kingdom, and colleagues evaluated 188 prepubertal, treatment-naive participants with GH deficiency from the PREDICT prospective long-term follow-up study to determine the effect of living at different latitudes on height velocity (cm per year) and the interaction of environmental and genomic factors in response to recombinant human growth hormone (rhGH) treatment.

Peter Clayton

Peter Clayton

The effect of treatment with rhGH during a year was measured by relating height velocity to summer daylight exposure, the carriage of seven single nucleotide polymorphisms (SNPs) previously linked to high growth response and basal gene expression before treatment.

A better height velocity in response to rhGH was found among participants from latitudes with higher summer daylight exposure compared with those from latitudes with intermediate and lower summer daylight exposure (P = .019). Summer daylight exposure was correlated with height velocity among all groups (P = .006).

SNP and summer daylight exposure in relation to growth response showed a significant interaction for SNPs within GRB10, IGFBP3, TGF-alpha, CYP19A1 and TP53 genes (P < .05).

SNPs in IGFBP3, TGF-alpha and TP53 had a greater effect on height velocity in participants from higher summer daylight exposure locations, the opposite was found for GRB10 and CYP19A1.

“The transcriptional regulator NANOG was found to be a master regulator of these interactions implicated in the development of circadian oscillator action and bone growth,” the researchers wrote. — by Amber Cox

Reference:

De Leonibus C, et al. Poster PP03-3. Presented at: The Endocrine Society Annual Meeting; March 5-8, 2015; San Diego.

Disclosure: Clayton reports financial ties to Merck. The study was funded in part by Merck.