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Interrelationship between insulin, leptin and growth hormone in growth hormone-treated children
Z Zadik1, I Wittenberg, N Segal
1Pediatric Endocrine Unit, Kaplan Medical Center, Rehovot, Israel. zadikz@netvision.net.il
Insights
Growth hormone (GH) therapy in obese children did not alter insulin sensitivity. Leptin levels decreased, inversely correlating with initial values and body mass reduction, but did not increase with insulin dosage.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Hormone Therapy
Background:
- Obesity in children is associated with insulin resistance and altered leptin levels.
- Growth hormone (GH) therapy is used for various pediatric conditions, but its metabolic effects in obese children require further investigation.
Purpose of the Study:
- To evaluate insulin homeostasis during GH therapy in obese children.
- To assess the impact of GH treatment on insulin and leptin concentrations in this population.
Main Methods:
- A 3-month study involving 19 obese children (8 with Prader-Willi Syndrome) receiving GH (0.1 IU/kg/day).
- Comparison groups included 29 non-treated obese children and 49 GH-treated non-obese short children.
- Measurements included leptin, insulin sensitivity index, and insulin response to intravenous glucose tolerance test (IVGTT).
Main Results:
- Leptin concentration decreased significantly, inversely correlated with initial leptin and decreased body mass.
- Insulin sensitivity index remained unchanged during GH therapy.
- The decrease in leptin correlated inversely with the increase in first-phase insulin response to IVGTT.
- GH-treated subjects showed a higher glucose increase post-glucose load compared to untreated subjects.
Conclusions:
- GH therapy in obese children did not impair insulin sensitivity.
- Observed insulin responses were appropriate for glucose levels.
- GH treatment led to decreased leptin levels without increasing insulin concentrations, contrary to initial hypotheses.
Objectives:
The aim of the study was to examine insulin homeostasis during growth hormone (GH) therapy, and to investigate the effect of GH treatment on insulin and leptin concentration in obese children.
Subjects:
Nineteen obese children (8 with Prader-Willi Syndrome (PWS)) were treated with GH 0.1 IU/kg/day dose for 3 months and were compared with 29 non-treated age and sex matched obese children (9 PWS) and 49 GH treated non-obese short children. Mean age of the children was 10.3+/-1.8 (6.7-13.8) y, with body mass index of 23.6+/-10.4 (11.5-47) kg/m2.
Results:
Leptin concentration decreased and was correlated inversely with initial leptin value (r2=-0.374, P<0.001) and decreased body mass (r2=0.338, P=0.001). Insulin sensitivity index was not significantly changed during therapy. Leptin decrease after 3 months of GH administration was correlated inversely with the increase in first phase insulin response to intravenous glucose tolerance test (IVGTT) (r2=-0.595, P<0.001). Results of long-term follow-up of treated patients demonstrated a decrease in insulin concentration after cessation of therapy. In GH-treated subjects, the glucose increase in response to glucose load appeared to be higher than in untreated subjects.
Conclusion:
The high insulin response to glucose load seen in GH-treated subjects was appropriate to their glucose concentration and the insulin sensitivity index was unchanged relative to the pretreatment period. Increased insulin dosage in our patients did not induce an increase in leptin concentrations as had been hypothesised.