ESPE Abstracts (2016) 86 RFC14.7

GH Influences Plasma Fasting Adropin Concentration in Patients with Turner Syndrome

Beata Wikieraa, Magdalena Krawczykb, Anna Noczynskaa & Jacek Daroszewskic


aDepartment of Endocrinology, Diabetology for Children and Adolescents, Wroclaw Medical University, Wroclaw, Poland; bFourth Military Hospital, Wroclaw, Poland; cDepartment of Endocrinology, Diabetes and Isotope Therapy, Wroclaw Medical University, Wroclaw, Poland


Background: Increased adiposity and insulin resistance are conditions frequently observed nowadays. Many hormones are involved in the pathogenesis of the condition but therapeutic options we can offer to the patients are still scant. Each newly discovered peptide give us hope. Adropin (Ad) is a newly discovered metabolic hormone involved in energy homeostasis. This homeostasis is frequently disturbed in patient with Turner Syndrome (TS). Patient with Turner syndrome are unique model for studies of an effect of the treatment with supraphysiological doses of growth hormone (GH)

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

Method: The study group consisted of 36 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: adropin, OGTT, insulin, lipids, IGF-1, and IGFBP-3.

Results: The increase of IGF-1 concentration at the end of observation was significant (from 119.4±62.46 to 413.37±204.38 ng/ml, mean±S.D., P=0.000). 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). rGH treatment cause a significant rise in Ad level. The correlation between adropin and IGF-1 and IGF-1 SDS levels was not significant neither before nor on the treatment (r=0.17 and r=0.04 respectively). Adropin concentration correlated with IGFBP3 level before rGH treatment but not on rGH therapy. Ad also correlated with insulin level before GH applying. Correlation with glucose levels at 30’ of OGTT was stable and even rise on GH treatment (P=0.33 vs P=0.48). Similar observation was noticed for lipids, but close correlations between Ad adropin and total cholesterol, LDL cholesterol, triglycerides (TG) before GH applying changed on rGH therapy. The only correlation noticed in GH treated patients was between Ad adropin and TG (P=0.34).

Conclusion: Result of the study showed an increase in adropin level following rGH application is not mediated by IGF-1. rGH treatment changes adropin influence on lipid metabolism, but ameliorates insulin action.

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