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Investigation of Mechanisms for Transmission of Impaired Glucose Metabolism in Infants Exposed to Diabetes in Utero — IMAGINE  

Pregnancy Clinical Trial

Official title:
Investigation of Mechanisms for Transmission of Impaired Glucose Metabolism in Infants Exposed to Diabetes in Utero

Clinical Trial Summary

This proposed study; Investigation of mechanisms for transmission of impaired glucose metabolism in infants exposed to diabetes in utero, will test the overarching hypothesis that impaired maternal substrate oxidation (metabolic inflexibility) and placental lipotoxicity are characteristics of diabetic pregnancies and in utero development within these conditions programs a metabolically inflexible phenotype in the offspring.

Clinical Trial Description

This translational research study will obtain paired measures of metabolic flexibility (postprandial RQ minus basal RQ) in response to a standardized meal by indirect calorimetry in mother:infant dyads of diabetic and non-diabetic pregnancies. The downstream effects of the intrauterine exposure to diabetes and gestational lipotoxicity will be tested in the infant: 1) at birth by studying adipogenic pathways and mitochondrial function in umbilical cord mesenchymal stem cells cultured in myogenic conditions[13], and 2) by studying metabolic flexibility in the infant in a whole body infant calorimeter in response to a standardized meal. Mothers will be enrolled between (33-35 weeks of gestation) and their infants will be enrolled between 10-30 days of life with the following aims. Aim 1. Characterize metabolic flexibility and lipotoxicity in diabetic and non-diabetic pregnancies. Hypothesis 1A: In response to a standardized meal in late pregnancy, diabetic pregnancies will be metabolically inflexible (blunted switch in RQ from the fasted state to the postprandial state) compared to non-diabetic pregnancies matched for maternal age and pregravid BMI. Hypothesis 1B: Placenta from diabetic pregnancies will have higher lipid content, reduced mitochondrial content and lower rates of mitochondrial oxygen consumption compared to placenta from non-diabetic pregnancies. Aim 2. Test whether intrauterine exposure to maternal diabetes infers disordered substrate oxidation in offspring at birth (in myocytes cultured from umbilical cord mesenchymal stem cells) and early in postnatal life (metabolic flexibility in response to a standardized meal). Hypothesis 2A: Umbilical cord mesenchymal stem cells cultured in myogenic conditions from diabetic pregnancies will have greater lipid content, reduced mitochondrial content, and lower rates of mitochondrial electron transport oxygen consumption and fatty acid oxidation. Hypothesis 2B: In response to a standardized meal, offspring of diabetic pregnancies will be metabolically inflexible (blunted switch in RQ from the pre- to postprandial state) compared to offspring of non-diabetic pregnancies. ;

Study Design

Related Conditions & MeSH terms

Clinical Trial Details
NCT number NCT02926079
Study type Observational
Source Pennington Biomedical Research Center
Contact
Status Completed
Phase
Start date May 23, 2017
Completion date January 8, 2019
View Details
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