ESPE Abstracts

Introduction: Brown adipose tissue (BAT) secretes molecules capable of modulating systemic metabolism. Growth hormone (GH) has hyperglycemic action, produces lipolysis and increases muscle mass. However, there are no human studies on its effect on the BAT and lipidome.

Aim: To evaluate the effect of GH on BAT and lipidome in small for gestational age (SGA) patients and its relationship with adherence to treatment.

Material and methods: Eleven prepubertal SGA patients between 3-9 years of age were recruited. They were classified into two groups: a) treated with GH (SGA-GH: 7 patients) and b) not treated with GH (SGA: 4 patients). The indicated GH was somatropin (Saizen® from Merck-Serono) using the EasyPodSystem device at a dose of 0.035mg/kg/day. A baseline visit to all patients and follow-up were done in the SGA-GH group at 3 and 12 months of treatment. At each visit (baseline, 3 and 12 months post-treatment) anthropometric and adherence data were collected using the EasypodConnect® app, as well as a fasting blood sample. Basic blood count and biochemistry, hormone levels, and concentrations of molecules of interest were measured. The thermogenic capacity of the supraclavicular BAT was also determined by infrared thermography after cold stimulation. Finally, a lipidomic analysis by mass spectrometry was performed on the serum of these patients. Statistical analysis was performed using IBMSPSS-Statistics19.0.

Results: The adherence to GH was correct. At the lipidomic level, 42 lipid species appeared modulated in SGA vs. SGA-GH at baseline. SGA-GH group showed increased levels of odd-chain fatty acids (OCSFAs) that are associated with cardiovascular protection. Some lipid species related to cellular senescence appeared elevated in the SGA-GH serum after the treatment. After GH treatment, there was a trend of increasing concentrations of CXCL14, FGF21, IL-8, leptin, and MCP1, and a slight decrease in GDF15, adiponectin, and resistin. The SGA group showed lower basal resting temperature of the supraclavicular BAT than the SGA-GH group. Treatment with GH did not produce remarkable changes in the thermogenic capacity except in one patient whose low growth response to GH coincided with a worsening of the thermogenic capacity of BAT.

Conclusions: GH treatment increases some lipid species related to cardiovascular protection and markers of cellular senescence. This study opens a door about the GH effect on BAT activity by modulating the levels of some batokines with a systemic effect.