Serum IGF1 and linear growth in children with congenital leptin deficiency before and after leptin substitution
| Autor: | Heike Vollbach, Shlomit Shalitin, Ingrid Körber, Marianna Beghini, Katja Kohlsdorf, Werner F. Blum, Julia von Schnurbein, Belinda Lennerz, Ferruccio Santini, Martin Wabitsch, Christian Denzer, Stephanie Brandt |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Molar Leptin Male medicine.medical_specialty Adolescent Endocrinology Diabetes and Metabolism IGFBP3 Medicine (miscellaneous) 030209 endocrinology & metabolism Article Cohort Studies 03 medical and health sciences Metreleptin chemistry.chemical_compound 0302 clinical medicine Weight loss Internal medicine medicine Humans Obesity Insulin-Like Growth Factor I Child Nutrition and Dietetics business.industry Infant Endocrine system and metabolic diseases medicine.disease 030104 developmental biology Endocrinology chemistry Child Preschool Female medicine.symptom Linear growth business Deficiency Diseases hormones hormone substitutes and hormone antagonists Cohort study |
| Zdroj: | International Journal of Obesity (2005) |
| Popis: | Background Evidence from in vitro and rodent studies suggests that leptin, a key signal of long-term energy reserves, promotes IGF1 synthesis and linear growth. This effect of leptin has not been fully investigated in humans. The aim of our study was to investigate the effect of leptin substitution on growth factors and linear growth in children with congenital leptin deficiency (CLD). Methods In this cohort study we included eight pediatric patients (six males), age 0.9–14.8 years, who were diagnosed with CLD and received leptin substitution at our University Medical Center. We calculated standard deviation scores (SDS) for serum levels of IGF1 and IGFBP3, IGF1/IGFBP3 molar ratio, and height at baseline (T0) and 12 months (T12) after the initiation of substitution with metreleptin. Results All patients had severe obesity (BMI-SDS mean ± SD: 4.14 ± 1.51) at T0 and significant BMI-SDS reduction to 2.47 ± 1.05 at T12. At T0, all patients were taller than the mid-parental median, yet had low IGF1 and IGF1/IGFBP3 molar ratios (IGF1-SDS$$\overline x$$ x ¯ T0: −1.58 ± 0.92, IGF1/IGFBP3 molar ratio-SDS$$\overline x$$ x ¯ T0: −1.58 ± 0.88). At T12, IGF1-SDS increased significantly (∆T0–12: 1.63 ± 1.40, p = 0.01), and IGFBP3-SDS and IGF1/IGFBP3 molar ratio-SDS showed a trend toward an increase. In the three children within the childhood growth period (post-infancy, pre-puberty) height-SDS increased (∆height-SDST0–12: 0.57 ± 0.06, p = 0.003) despite substantial weight loss. Conclusions These results in CLD patients are contrary to observations in children with idiopathic obesity who typically have above-mean IGF1 levels that decrease with weight loss, and therefore suggest that leptin increases IGF1 levels and promotes linear growth. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|