Nora E Grotenfelt1, Niko S Wasenius2,3, Kristiina Rönö4, Hannele Laivuori4,5,6, Beata Stach-Lempinen7, Marju Orho-Melander8, Christina-Alexandra Schulz8, Hannu Kautiainen3,9, Saila B Koivusalo4, Johan G Eriksson2,3,10. 1. Folkhälsan Research Centre, Biomedicum Helsinki, University of Helsinki, Haartmaninkatu 8, P.O. Box 63, 00014, Helsinki, Finland. nora.grotenfelt@helsinki.fi. 2. Folkhälsan Research Centre, Biomedicum Helsinki, University of Helsinki, Haartmaninkatu 8, P.O. Box 63, 00014, Helsinki, Finland. 3. Department of General Practice and Primary Health Care, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 4. Department of Obstetrics and Gynecology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 5. Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland. 6. Department of Medical and Clinical Genetics, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. 7. Department of Obstetrics and Gynecology, South-Karelia Central Hospital, Lappeenranta, Finland. 8. Department of Clinical Sciences in Malmö, Lund University Diabetes Center, Lund University, Lund, Sweden. 9. Department of General Practice and Primary Health Care, University of Eastern Finland, Kuopio, Finland. 10. Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland.
Abstract
AIMS/HYPOTHESIS: The aim of this study was to assess the interaction between melatonin receptor 1B gene (MTNR1B) rs10830963 polymorphism and lifestyle intervention during pregnancy on occurrence of gestational diabetes mellitus (GDM) in high-risk women. METHODS: This is a secondary analysis of the randomised controlled gestational diabetes prevention trial 'RADIEL', conducted between 2008 and 2014 in four maternity hospitals in southern Finland. A total of 226 women with a history of GDM and/or a pre-pregnancy BMI ≥ 30 kg/m(2) were enrolled at <20 weeks of gestation (mean 13 weeks) and randomised into an intervention group receiving counselling on diet, physical activity and weight control and a control group receiving standard antenatal care. The main outcome was incidence of GDM, defined as one or more pathological glucose values in a standard 75 g 2-h OGTT. The MTNR1B rs10830963 was genotyped for further analyses. RESULTS: No significant differences were found in the genotype distribution between the intervention and the control group. A significant interaction was observed between the rs10830963 genotypes and the lifestyle intervention on age-adjusted occurrence of gestational diabetes (p = 0.038). Among women homozygous for the C allele of rs10830963, the OR for GDM was significantly lower in the intervention group than in the control group (OR 0.16 [95% CI 0.03, 0.85], p = 0.014). This difference was not seen in women heterozygous (OR 0.88 [95% CI 0.32, 2.41], p = 0.798) or homozygous (OR 2.25 [95% CI 0.34, 14.69], p = 0.384) for the risk allele G. CONCLUSIONS/ INTERPRETATION: In women at high risk of GDM, only those not carrying the risk allele G benefited from the lifestyle intervention. Our results indicate that certain genetic risk variants may modify the effectiveness of lifestyle interventions. This may provide important information when planning GDM prevention studies in the future.
RCT Entities:
AIMS/HYPOTHESIS: The aim of this study was to assess the interaction between melatonin receptor 1B gene (MTNR1B) rs10830963 polymorphism and lifestyle intervention during pregnancy on occurrence of gestational diabetes mellitus (GDM) in high-risk women. METHODS: This is a secondary analysis of the randomised controlled gestational diabetes prevention trial 'RADIEL', conducted between 2008 and 2014 in four maternity hospitals in southern Finland. A total of 226 women with a history of GDM and/or a pre-pregnancy BMI ≥ 30 kg/m(2) were enrolled at <20 weeks of gestation (mean 13 weeks) and randomised into an intervention group receiving counselling on diet, physical activity and weight control and a control group receiving standard antenatal care. The main outcome was incidence of GDM, defined as one or more pathological glucose values in a standard 75 g 2-h OGTT. The MTNR1Brs10830963 was genotyped for further analyses. RESULTS: No significant differences were found in the genotype distribution between the intervention and the control group. A significant interaction was observed between the rs10830963 genotypes and the lifestyle intervention on age-adjusted occurrence of gestational diabetes (p = 0.038). Among women homozygous for the C allele of rs10830963, the OR for GDM was significantly lower in the intervention group than in the control group (OR 0.16 [95% CI 0.03, 0.85], p = 0.014). This difference was not seen in women heterozygous (OR 0.88 [95% CI 0.32, 2.41], p = 0.798) or homozygous (OR 2.25 [95% CI 0.34, 14.69], p = 0.384) for the risk allele G. CONCLUSIONS/ INTERPRETATION: In women at high risk of GDM, only those not carrying the risk allele G benefited from the lifestyle intervention. Our results indicate that certain genetic risk variants may modify the effectiveness of lifestyle interventions. This may provide important information when planning GDM prevention studies in the future.
Entities:
Keywords:
Clinical trial; Diabetes; Gestational; MT2; Melatonin; Polymorphism; Pregnancy; Prevalence; Public health; Receptor; Single nucleotide
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