ESPE Abstracts (2015) 84 P-2-255

ESPE2015 Poster Category 2 Diabetes (60 abstracts)

Significant Impact of Nocturnal Melatonin Secretion on Obesity-Related Metabolic Disorders in Children and Adolescents

Johanna Overberg a , Peter Kühnen a , Andrea Ernert b , Heiko Krude a & Susanna Wiegand a


aDepartment of Pediatric Endocrinology and Diabetology, Charité Children’s Hospital, Universitätsmedizin Berlin, Berlin, Germany; bDepartment of Biometry and Clinic Epidemiology, Charité Universitätsmedizin Berlin, Berlin, Germany


Background: In addition to its function in circadian rhythm Melatonin plays an important role in energy metabolism and body weight regulation. In animals pinealectomy induces insulin resistance and administration of melatonin to diabetes prone rats ameliorates their glucose metabolism. Furthermore loss-of-function mutations of the melatonin receptor gene are associated with insulin resistance and DM II in humans.

Objective and hypotheses: So far the effect of melatonin on energy metabolism in childhood remains unclear. As obese adolescents were found to have disturbed and shifted sleep rhythm a link between low melatonin secretion and impaired glucose metabolism was suggested. We therefore aimed to explore the effect of nocturnal melatonin secretion on glucose metabolism in obese children and adolescents.

Method: We performed a cross sectional study of 148 obese (>97.percentile) children and adolescences (10–17 years). Based on fasting blood samples, insulin resistance was defined as age and sex adjusted R-HOMA >95. percentile (using Allard percentiles) and correlated with nocturnal Melatonin secretion. Melatonin secretion was measured as its main metabolite 6-sultatoxymelatonin normalized to urinary creatinine in the first morning urinary void.

Results: Subjects with insulin resistance (n=101) showed significant lower nocturnal melatonin levels (P=0,004). The median ratio of 6-sulfatoxymelatonin to creatinine was 24.3 ng/mg (1st quartile =15.7 ng/mg; 3rd quartile=33.0 ng/mg) among subjects with insulin resistance vs 32.8 ng/mg (1st quartile=23.1 ng/mg; 3rd quartile=42.7 ng/mg) among those with unimpaired insulin secretion. Adjusted for age, sex and Tanner status the effect remained significant.

Conclusion: We found a strong association of lower nocturnal melatonin secretion and insulin resistance in obese children. To increase melatonin levels – either endogenously by prolonged nighttime darkness or exogenously by supplementation – might be one future strategy in management of obesity-induced morbidity.

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