ESPE Abstracts (2015) 84 P-1-86

aDepartment of Endocrinology and Diabetology for Children and Adolescents, Wroclaw Medical University, Wroclaw, Poland; bDepartment of Endocrinology, Diabetes and Isotope Therapy, Wroclaw Medical University, Wroclaw, Poland

Background: Brown adipose tissue metabolism is of remarkable pathophysiological interest, because it could be a target for therapies for obesity and metabolic syndrome. Irisin (Ir), recently identified adipomyokine is essential in a white-to-brown fatty tissue transdifferentiation, and mediates some of the positive influences on metabolic disorders through increase of energy expenditure. The exact regulation of Ir secretion and action is unknown but positive associations of circulating Ir with growth hormone and IGF1 were found.

Objective and hypotheses: We studied Ir response in a group of patients treated with supraphysiological doses of growth hormone (rGH).

Method: The study group consisted of 36 turner syndrome (TS) patients aged 3.2–16.07 years (mean 8.2 years) diagnosed by karyotyping. The rGH was applied in a dose 0.05 mg/kg per day prior to and following the treatment anthropometrical data were recorded as well as biochemical parameters were measured: Ir, OGTT, insulin, IGF1, and IGFBP3.

Results: The increase of IGF1 concentration at the end of observation was significant (from 119.4±62.46 to 413.37±204.38 ng/ml, mean±SD, P=0.000). The rise of Ir level was recorded on rGH treatment (2.1±1.03 vs 2.47±0.79 μg/ml, mean±SD, P=0.035). The GH treatment influenced insulin resistance revealed by increased HOMA values (median 0.64±0.45 before and 0.92±0.97 after, P=0.02). The correlation between Ir and IGF1 levels was not significant neither before nor on the treatment (P=0.22 and P=0.95 respectively). At the end of observation Ir was negatively related to % weight to height ratio (P=0.04). The correlation between Ir and insulin (r=−0.44, P=0.01) and Ir and HOMA (r=−0.46, P=0.007) was significant.

Conclusion: Result of the study showed an increase in Ir level following GH application. It seems to be not IGF1 mediated. Ir may mediate some metabolic effects of GH treatment. We are unable to conclude whether Ir rise is connected with direct GH stimulation, their influence of body composition, or with altered insulin sensitivity.

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