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Maternal Gestational Glucose Concentration Is Associated with Offspring Insulin Sensitivity and β-Cell Function in Children Aged 5-10 Years

« Back to Volume 26, Issue 1, September 2010 - Table of Contents

From ENDO 2010 The Endocrine Society Annual Meeting, San Diego, June 19-22, 2010

Evidence suggests that intrauterine exposure to elevated glucose concentrations may be a mediating factor in prenatal programming of offspring disease risk. However, studies examining the effects of maternal glucose concentration on robust measures of insulin sensitivity and β-cell response in prepubertal children are limited. Therefore, the objective of this study was to determine the associations of maternal glucose concentration with robust and physiologic measures of insulin sensitivity and β-cell response. Participants were 21 children aged 5-10 years. Children's insulin sensitivity index (SI) and measures of basal, static, dynamic, and total β-cell response were determined by mathematical modeling using insulin, glucose, and c-peptide values following a liquid meal tolerance test. Dual-energy X-ray absorptiometry (DEXA) was used for the determination of children's percent total body fat (%BF). Maternal glucose concentration was determined following a 50-gram, 1-hour oral glucose challenge test at 24-28 weeks of gestation and ranged from 75-229 mg/dL. Independent associations of maternal glucose with SI and β-cell response indices were determined by multiple linear regression analyses. Maternal glucose concentration was significantly, inversely associated with SI, independent of %BF (Parameter Estimate + SE: -0.88+0.27, P<0.01). A significant, positive association was observed for maternal glucose concentration with static β-cell response, independent of %BF and SI (Parameter Estimate + SE: 1.12+0.41, P<0.05).

Maternal glucose concentration significantly impacted insulin sensitivity and β-cell response, independent of adiposity, in offspring at 5-10 years of age. These results suggest that fetal programming occurs both at the pancreas and at the level of insulin target tissues such as skeletal muscle and liver.

Bush NC, Chandler-Laney PC, Granger WM, Rouse DJ, Gower BA. University of Alabama at Birmingham, Birmingham, Alabama, USA and Brown University, Providence, Rhode Island, USA

Editor's Comment

Maternal glucose concentration in pregnancy appears to be a strong epigenetic factor for fetal programming which impacts insulin sensitivity in offspring during childhood. Perhaps this effect may be imprinted for life.¹ There is growing evidence that even mild gestational diabetes mellitus (GDM) significantly increases the risk of a number of short- and long-term adverse consequences² for the fetus and mother, including a predisposition to the development of metabolic syndrome and type 2 diabetes. Maternal and childhood obesity, as well as cardiovascular disease, are also potential long-term consequences of GDM. On the other hand, there is a growing body of evidence suggesting that the risk of many of these consequences can be significantly reduced or eliminated by aggressive treatment of all types of diabetes - including mild GDM.³ However, there remains, a great deal of controversy over when to begin screening for hyperglycemia in pregnancy and at what level of hyperglycemia aggressive intervention should be initiated.^4-5

Fima Lifshitz, MD

References - (linked to )

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Last Updated: 2/2/2011