Bojan Tubic1, Per Magnusson2, Staffan Mårild3, Monica Leu4, Verena Schwetz5, Isabelle Sioen6, Diana Herrmann7, Barbara Obermayer-Pietsch8, Lauren Lissner9, Diana Swolin-Eide10. 1. Department of Pediatrics, Institute of Clinical Sciences, The Queen Silvia Children's Hospital, The Sahlgrenska Academy at the University of Gothenburg, SE-416 85 Göteborg, Sweden. Electronic address: bojan.tubic@gu.se. 2. Department of Clinical Chemistry and Department of Clinical and Experimental Medicine, Linköping University, SE-581 85, Linköping, Sweden. Electronic address: per.magnusson@regionostergotland.se. 3. Department of Pediatrics, Institute of Clinical Sciences, The Queen Silvia Children's Hospital, The Sahlgrenska Academy at the University of Gothenburg, SE-416 85 Göteborg, Sweden. Electronic address: staffan.marild@pediat.gu.se. 4. Section for Epidemiology and Social Medicine (EPSO), Department of Public Health and Community Medicine, The Sahlgrenska Academy at University of Gothenburg, Box 454, SE-405 30 Göteborg, Sweden. Electronic address: monica.leu@gu.se. 5. Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria. Electronic address: verena.schwetz@medunigraz.at. 6. Department of Public Health, Ghent University, De Pintelaan 185, B-9000 Gent, Belgium; Research Foundation, Flanders, Brussels, Belgium. Electronic address: isabelle.Sioen@ugent.be. 7. Leibniz Institute for Prevention Research and Epidemiology, BIPS, Achterstr. 30, DE-28359, Bremen, Germany. Electronic address: herrmann@bips.uni-bremen.de. 8. Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, A-8036, Graz, Austria. Electronic address: barbara.obermayer@medunigraz.at. 9. Section for Epidemiology and Social Medicine (EPSO), Department of Public Health and Community Medicine, The Sahlgrenska Academy at University of Gothenburg, Box 454, SE-405 30 Göteborg, Sweden. Electronic address: lauren.lissner@gu.se. 10. Department of Pediatrics, Institute of Clinical Sciences, The Queen Silvia Children's Hospital, The Sahlgrenska Academy at the University of Gothenburg, SE-416 85 Göteborg, Sweden. Electronic address: diana.swolin-eide@vgregion.se.
Abstract
OBJECTIVE: Osteocalcin (OC), an aboundant non-collagenous bone protein, is inversely associated with parameters of glucose metabolism. Interactions between bone tissue and energy metabolism have not been thoroughly investigated during childhood. This study investigated OC, metabolic parameters and anthropometric characteristics in normal weight and overweight/obese children. METHODS: This study comprised 108 (46 normal weight/62 overweight/obese) Swedish 2-9year old children. Anthropometric data, insulin, glucose, glycosylated haemoglobin (HbA1c), HOMA index, vitamin D, adiponectin, total OC, carboxylated OC (cOC) and undercarboxylated OC (ucOC) were analysed. RESULTS: No difference was found for total OC between the normal and overweight/obese groups, with a mean (±SD) value of 82.6 (±2.8) ng/mL and 77.0 (±2.4) ng/mL, (P=0.11), respectively. Overweight children had lower cOC levels, mean 69.1 (±2.2) ng/mL, vs. normal weight children, mean 75.6 (±2.5) ng/mL (P=0.03). The mean ucOC levels of 7.9 (±0.4) ng/mL in overweight children did not differ vs. normal weight children, mean level 7.0 (±0.4) ng/mL, (P=0.067). None of the three OC forms correlated with any of the measured parameters. CONCLUSIONS: The cOC levels were lower in overweight children. There was no correlation between the three OC forms and any of the measured anthropometric or metabolic parameters. OC has been suggested to have a possible metabolic role, but in general the current study in prepubertal children does not support the hypothesis of an association between OC and a positive metabolic profile.
OBJECTIVE:Osteocalcin (OC), an aboundant non-collagenous bone protein, is inversely associated with parameters of glucose metabolism. Interactions between bone tissue and energy metabolism have not been thoroughly investigated during childhood. This study investigated OC, metabolic parameters and anthropometric characteristics in normal weight and overweight/obesechildren. METHODS: This study comprised 108 (46 normal weight/62 overweight/obese) Swedish 2-9year old children. Anthropometric data, insulin, glucose, glycosylated haemoglobin (HbA1c), HOMA index, vitamin D, adiponectin, total OC, carboxylated OC (cOC) and undercarboxylated OC (ucOC) were analysed. RESULTS: No difference was found for total OC between the normal and overweight/obese groups, with a mean (±SD) value of 82.6 (±2.8) ng/mL and 77.0 (±2.4) ng/mL, (P=0.11), respectively. Overweight children had lower cOC levels, mean 69.1 (±2.2) ng/mL, vs. normal weight children, mean 75.6 (±2.5) ng/mL (P=0.03). The mean ucOC levels of 7.9 (±0.4) ng/mL in overweight children did not differ vs. normal weight children, mean level 7.0 (±0.4) ng/mL, (P=0.067). None of the three OC forms correlated with any of the measured parameters. CONCLUSIONS: The cOC levels were lower in overweight children. There was no correlation between the three OC forms and any of the measured anthropometric or metabolic parameters. OC has been suggested to have a possible metabolic role, but in general the current study in prepubertal children does not support the hypothesis of an association between OC and a positive metabolic profile.
Authors: Kelly Virecoulon Giudici; Joseph M Kindler; Berdine R Martin; Emma M Laing; George P McCabe; Linda D McCabe; Dorothy B Hausman; Lígia Araújo Martini; Richard D Lewis; Connie M Weaver; Munro Peacock; Kathleen M Hill Gallant Journal: Nutr Metab (Lond) Date: 2017-03-07 Impact factor: 4.169