Literature DB >> 17635945

Insulin resistance in Hispanic large-for-gestational-age neonates at birth.

Jennifer Shine Dyer1, Charles R Rosenfeld, Julie Rice, Mark Rice, Dana S Hardin.   

Abstract

CONTENT: Intrauterine exposure to maternal diabetes and large size at birth are known risk factors for the subsequent development of insulin resistance and metabolic syndrome. Although Hispanic youth have been shown to have a high prevalence of metabolic syndrome, it is unknown whether metabolic abnormalities and a predisposition for glucose intolerance are present at birth.
OBJECTIVE: The objective of the study was to determine whether abnormalities in insulin sensitivity exist at or soon after birth in large-for-gestational-age neonates born to Hispanic women with and without gestational diabetes. DESIGN/PATIENTS/
SETTING: Forty-two term Hispanic neonates were enrolled for cross-sectional studies at 24-48 h after birth and included nine large-for-gestational-age neonates delivered of women with gestational diabetes (large-for-gestational-age-IDM), 12 large-for-gestational-age but not IDM neonates, 11 poorly grown (at the fifth to 10th percentile), and 10 appropriate-for-gestational-age neonates. Insulin sensitivity and secretion were measured by shortened fasting iv glucose tolerance test. MAIN OUTCOME MEASURE: Insulin sensitivity index was measured within 48 h of birth.
RESULTS: Neonates were studied at 36 +/- 11 h postnatally, and all groups were euglycemic at the time of study. However, insulin sensitivity was significantly lower (P < 0.05, ANOVA) in large-for-gestational-age-IDM [3.0 +/- 0.7 (sem) mU/liter.min] and large-for-gestational-age-non-IDM (2.2 +/- 0.4 mU/liter.min) cohorts in comparison with poorly grown (5.0 +/- 0.7 mU/liter.min) and appropriate-for-gestational-age controls (5.4 +/- 0.8 mU/liter.min). Insulin secretion did not differ between groups.
CONCLUSIONS: Reduced insulin sensitivity is present soon after birth in Hispanic large-for-gestational-age neonates born to mothers with and without gestational diabetes, demonstrating the onset of insulin resistance before birth and evidence of altered fetal programming.

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Year:  2007        PMID: 17635945     DOI: 10.1210/jc.2007-0079

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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