OBJECTIVEInfants born to mothers with gestational diabetes mellitus (GDM) are at greater risk of later adverse metabolic health. We examined plausible candidate mediators, adipose tissue (AT) quantity and distribution and intrahepatocellular lipid (IHCL) content, comparing infants of mothers with GDM and without GDM (control group) over the first 3 postnatal months. RESEARCH DESIGN AND METHODSWe conducted a prospective longitudinal study using MRI and spectroscopy to quantify whole-body and regional AT volumes, and IHCL content, within 2 weeks and 8-12 weeks after birth. We adjusted for infant size and sex and maternal prepregnancy BMI. Values are reported as the mean difference (95% CI). RESULTSWe recruited 86 infants (GDM group 42 infants; control group 44 infants). Mothers with GDM had good pregnancy glycemic control. Infants were predominantly breast-fed up to the time of the second assessment (GDM group 71%; control group 74%). Total AT volumes were similar in the GDM group compared with the control group at a median age of 11 days (228 cm 3 [95% CI 2121, 65], P = 0.55), but were greater in the GDM group at a median age of 10 weeks (247 cm 3 [56, 439], P = 0.01). After adjustment for size, the GDM group had significantly greater total AT volume at 10 weeks than control group infants (16.0% [6.0, 27.1], P = 0.002). AT distribution and IHCL content were not significantly different at either time point. CONCLUSIONSAdiposity in GDM infants is amplified in early infancy, despite good maternal glycemic control and predominant breast-feeding, suggesting a potential causal pathway to later adverse metabolic health. Reduction in postnatal adiposity may be a therapeutic target to reduce later health risks.Diabetes in pregnancy is increasing and currently affects up to 5% of women in the U.K.(1) and up to 9.2% in the U.S. (2). Approximately 87.5% of cases are gestational diabetes mellitus (GDM), 7.5% are type 1 diabetes, and 5% are type 2 diabetes (1). The offspring of mothers with diabetes have greater risks of adverse metabolic sequelae in childhood and later life that appear to be additional to genetic predisposition (3-5).The underlying mechanisms are unclear, but increased infant adiposity is a plausible mediator because adiposity in childhood and adult life are associated with type 2 diabetes and cardiovascular disease (6). The Hyperglycemia and Adverse

No abstract

BackgroundThe mechanisms responsible for the associations between very preterm birth and a higher risk of poor cardiovascular and metabolic health in adult life are unknown. MethodsComparison of the clinical and molecular phenotypes of healthy, normal weight young adults (18-27 years), born very preterm (<33 weeks gestational age (GA)) and at full-term (37-42 weeks GA).Outcomes included whole body magnetic resonance imaging; hepatic and muscle 1 H magnetic resonance spectroscopy; blood pressure (BP) measurement, urine and blood sampling and telomere length measurement. ResultsWe recruited 156 volunteers, 69 born very preterm (45 women; 24 men) and 87 born at full-term (45 women; 42 men). Preterm men had significantly more internal-abdominal adipose tissue (mean difference 0.33L (95% CI 0.04, 0.62), p<0.05), significantly fewer long telomeres (145-48.5kb: preterm men 14.1 ± 0.9%, term men 17.8 ± 1.1%, p<0.05; 48.5-8.6kb: preterm men 28.2 ± 2.6, term men 37.0 ± 2.4%, p<0.001) and a significantly higher proportion of shorter telomeres (4.2-1.3kb: preterm men 40•4 ± 3.5%, term men 29.9 ± 3.2%, p<0.01) compared to full-term men. ConclusionOur data indicate that healthy young adults born very preterm manifest clinical and molecular evidence of accelerated ageing.