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The GH-deficient children had significantly higher adiponectin (p<0.05) and total cholesterol (p<0.05) levels, and a significantly lower level of resistin (p<0.05) than the controls.

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Metabolic evaluation included measurements of adiponectin, resistin, IGF-1, total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), glucose, insulin, glycated haemoglobin (HbA1c), thyroid stimulating hormone (TSH) and free thyroxine (free T4) concentrations. 23 short age-matched children without growth hormone deficiency (GHD) or any genetic or chronic disorders were recruited as controls at baseline. This study investigated associations between the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis, adiponectin, resistin and metabolic profile in 47 GH-deficient children before and during 12 months of GH treatment.

(2017) confirmed that the baseline metabolic profile in GH-deficient children was not homogenous, and was better in GHdeficient children with low IGF-1 bioavailability expressed as the insulin-like growth factor-1/insulin-like growth factor binding protein-3 (IGF-1/IGFBP-3) molar ratio. Data concerning chang-es in the lipid profile, glucose homeostasis and thyroid function were also divergent (van der Sluis et al., 2002 Andersson et al., 2009 Smyczyńska et al., 2010 López-Siguero et al., 2011 Ciresi et al., 2016 Giavoli et al., 2017 Oświęcimska et al., 2017 Stawerska et al., 2017).

The discrepancy in the results of different studies evaluating the adipokine profile in untreated patients with GHD could be a result of varied metabolic panel reported in those children by several authors, who indicate that not all children with GHD have an impaired metabolic profile (Gleeson et al., 2007 López-Siguero et al., 2011 Meazza et al., 2014 Ciresi et al., 2016 Stawerska et al., 2017). This parameter may be potentially useful in diagnosing severe growth hormone deficiency in the adults. The degree of GH/IGF-1 axis disruption is related to the TAPN/FM. Severe, but not partial growth hormone deficiency impairs adiponectin production in the adipose tissue that is compensated by the increase of fat mass. In the subjects with normal GH secretion serum APN correlated positively with serum HDL cholesterol (r=0.28 p<0.05), and negatively with fasting blood glucose (r=-0.31 p<0.05). In patients with GHD positive correlations between APN and serum HDL cholesterol (r=0.39, p<0.05) have been demonstrated. After calculation of the total APN content in extracellular fluids per unit of fat tissue mass (TAPN/FM), these values were significantly lower in the SGHD (p<0.001) and correlated with the degree of impairment of the GH/IGF-1 axis functioning. There were no significant differences in the concentrations of APN between groups. Anthropometric measurements (height, weight, BMI), analysis of body composition and serum glucose, lipids, insulin, IGF-1 and APN assays were performed in all participants. The fourth examined group consisted of healthy individuals - H (46 participants 15 women, 31 men). The assessment of serum adiponectin levels in adolescents and young adults with severe or partial GHD and analysis of relationships between serum APN and GH/IGF-1 axis function impairment as well as cardiometabolic risk factors.īased on the results of insulin tolerance test (ITT) patients were qualified for one of the following groups: 1) severe GHD - SGHD (26 patients 8 women and 18 men) 2) partial GHD - PGHD (22 patients, 7 women and 15 men) 3) normal GH status - NGHS (28 patients, 9 women and 19 men). Growth hormone deficiency (GHD) may contribute to the development of disturbances in the hormonal function of adipose tissue (AT), and many disorders observed in untreated patients with GHD coincides with these contributed to low serum APN levels. Adiponectin (APN) is adipose tissue-derived hormone influencing energy metabolism.

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