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Aims/hypothesis: We aimed to assess associations between cord blood metabolic markers and fetal overgrowth, and whether cord markers mediated the impact of maternal adiposity on neonatal anthropometric outcomes among children born to Indigenous and Non-Indigenous Australian women with normal glucose tolerance (NGT), gestational diabetes mellitus (GDM) and pregestational type 2 diabetes mellitus. Methods: From the Pregnancy and Neonatal Outcomes in Remote Australia (PANDORA) study, an observational cohort of 1135 mother–baby pairs, venous cord blood was available for 645 singleton babies (49% Indigenous Australian) of women with NGT (n = 129), GDM (n = 419) and type 2 diabetes (n = 97). Cord glucose, triacylglycerol, HDL-cholesterol, C-reactive protein (CRP) and C-peptide were measured. Multivariable logistic and linear regression were used to assess the associations between cord blood metabolic markers and the outcomes of birthweight z score, sum of skinfold thickness (SSF), being large for gestational age (LGA) and percentage of body fat. Pathway analysis assessed whether cord markers mediated the associations between maternal and neonatal adiposity. Results: Elevated cord C-peptide was significantly associated with increasing birthweight z score (β 0.57 [95% CI 0.42, 0.71]), SSF (β 0.83 [95% CI 0.41, 1.25]), percentage of body fat (β 1.20 [95% CI 0.69, 1.71]) and risk for LGA [OR 3.14 [95% CI 2.11, 4.68]), after adjusting for age, ethnicity and diabetes type. Cord triacylglycerol was negatively associated with birthweight z score for Indigenous Australian women only. No associations between cord glucose, HDL-cholesterol and CRP >0.3 mg/l (2.9 nmol/l) with neonatal outcomes were observed. C-peptide mediated 18% (95% CI 13, 36) of the association of maternal BMI with LGA and 11% (95% CI 8, 17) of the association with per cent neonatal fat. Conclusions/interpretation: Cord blood C-peptide is an important mediator of the association between maternal and infant adiposity, across the spectrum of maternal glucose tolerance. [ABSTRACT FROM AUTHOR]

Background: In Australia's Northern Territory, 33% of babies are born to Indigenous mothers, who experience high rates of hyperglycemia in pregnancy. We aimed to determine the extent to which pregnancy outcomes for Indigenous Australian women are explained by relative frequencies of diabetes type [type 2 diabetes (T2DM) and gestational diabetes (GDM)].Methods: This prospective birth cohort study examined participants recruited from a hyperglycemia in pregnancy register. Baseline data collected were antenatal and perinatal clinical information, cord blood and neonatal anthropometry. Of 1135 women (48% Indigenous), 900 had diabetes: 175 T2DM, 86 newly diagnosed diabetes in pregnancy (DIP) and 639 had GDM. A group of 235 women without hyperglycemia in pregnancy was also recruited.Results: Diabetes type differed for Indigenous and non-Indigenous women (T2DM, 36 vs 5%; DIP, 15 vs 7%; GDM, 49 vs 88%, p < 0.001). Within each diabetes type, Indigenous women were younger and had higher smoking rates. Among women with GDM/DIP, Indigenous women demonstrated poorer birth outcomes than non-Indigenous women: large for gestational age, 19 vs 11%, p = 0·002; neonatal fat 11.3 vs 10.2%, p < 0.001. In the full cohort, on multivariate regression, T2DM and DIP were independently associated (and Indigenous ethnicity was not) with pregnancy outcomes.Conclusions: Higher rates of T2DM among Indigenous women predominantly contribute to absolute poorer pregnancy outcomes among Indigenous women with hyperglycemia. As with Indigenous and minority populations globally, prevention or delay of type 2 diabetes in younger women is vital to improve pregnancy outcomes and possibly to improve the long-term health of their offspring. [ABSTRACT FROM AUTHOR]

Background: Rates of diabetes in pregnancy are disproportionately higher among Aboriginal than non-Aboriginal women in Australia. Additional challenges are posed by the context of Aboriginal health including remoteness and disadvantage. A clinical register was established in 2011 to improve care coordination, and as an epidemiological and quality assurance tool. This paper presents results from a process evaluation identifying what worked well, persisting challenges and opportunities for improvement. Methods: Clinical register data were compared to the Northern Territory Midwives Data Collection. A cross-sectional survey of 113 health professionals across the region was also conducted in 2016 to assess use and value of the register; and five focus groups (49 healthcare professionals) documented improvements to models of care. Results: From January 2012 to December 2015, 1,410 women were referred to the register, 48% of whom were Aboriginal. In 2014, women on the register represented 75% of those on the Midwives Data Collection for Aboriginal women with gestational diabetes and 100% for Aboriginal women with pre-existing diabetes. Since commencement of the register, an 80% increase in reported prevalence of gestational diabetes among Aboriginal women in the Midwives Data Collection occurred (2011–2013), prior to adoption of new diagnostic criteria (2014). As most women met both diagnostic criteria (81% in 2012 and 74% in 2015) it is unlikely that the changes in criteria contributed to this increase. Over half (57%) of survey respondents reported improvement in knowledge of the epidemiology of diabetes in pregnancy since establishment of the register. However, only 32% of survey respondents thought that the register improved care-coordination. The need for improved integration and awareness to increase use was also highlighted. Conclusion: Although the register has not been reported to improve care coordination, it has contributed to increased reported prevalence of gestational diabetes among high risk Aboriginal women, in a routinely collected jurisdiction-wide pregnancy dataset. It has therefore contributed to an improved understanding of epidemiology and disease burden and may in future contribute to improved management and outcomes. Regions with similar challenges in context and high risk populations for diabetes in pregnancy may benefit from this experience of implementing a register. [ABSTRACT FROM AUTHOR]

Aboriginal and Torres Strait Islander women have high rates of gestational diabetes (GDM). The Pregnancy And Neonatal Diabetes Outcomes in Remote Australia (PANDORA) study is a prospective longitudinal cohort of women with type 2 diabetes (T2D), GDM or normoglycemia in pregnancy in the Northern Territory, Australia. In this analysis we report progression to prediabetes and T2D at 2.5 years [range 2.1, 3] postpartum in a subgroup of Aboriginal and Europid women with GDM and normoglycemia in pregnancy (n=337). Women with pre-existing T2D were excluded. Data were analysed using Fisher's exact tests. Among Aboriginal women with GDM we assessed predictions for progression using multivariate logistic regression. Aboriginal women with GDM (n=111) were younger than Europid women with GDM (n=104) (29 years (SD 5.9) vs. 32 (5.6) p<0.01), with similar first trimester BMI (28.9 kg/m2 (SD 7.2) vs. 28.5 (6.7) p=0.64). Of Aboriginal women with GDM, 24 (22%) progressed to T2D and 12 (11%) to prediabetes. Of Aboriginal women with normoglycemia (n=60), 1 (2%) progressed to T2D and 1 (2%) to prediabetes (p<0.01 for combined outcome vs. GDM women). Of Europid women with GDM, none progressed to T2D and 4 (4%) to prediabetes and of those with normoglycemia (n=62) none progressed to diabetes or prediabetes (p=0.09 vs. GDM women). Among Aboriginal women with GDM, factors associated with postpartum diabetes or prediabetes were age (OR 1.11, 1.03-1.2) and, after adjusting for age: severity of GDM (higher fasting plasma glucose (per 1 mmol/L OR 2.11, 1.23-3.62), use of insulin (OR 3.20, 1.35-7.6)) and higher first trimester BMI (per 3 kg/m2 OR 1.22, 1.01-1.47). Not smoking was protective (OR 0.35, 0.14-0.90), although any breastfeeding at 6-months postpartum was not (OR 0.95, 0.36-2.47). To our knowledge this is the only prospective study of Aboriginal and Torres Strait Islander women with GDM. We report the highest rates in the world of T2D after GDM at 2.5 years postpartum, highlighting a need for targeted interventions in this high-risk population. Disclosure: A. Wood: None. J. Boyle: None. F. Barzi: None. E.L. Barr: None. M.J.I. Hare: None. A. Titmuss: None. E. Death: None. M. Kirkwood: None. A. Simmonds: None. E.M. Moore: None. J. Oats: None. D. McIntyre: Other Relationship; Self; Novo Nordisk A/S. P.Z. Zimmet: None. A.D. Brown: None. J.E. Shaw: Advisory Panel; Self; AstraZeneca, Merck Sharp & Dohme Corp., Mylan, Sanofi. Research Support; Self; AstraZeneca. Speaker's Bureau; Self; Eli Lilly and Company, Mylan. L.J. Maple-Brown: None. [ABSTRACT FROM AUTHOR]