• Clinical and Experimental Pediatrics
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• v.49 no.9
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• pp.966-971
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• 2006

Purpose : 'Programming' describes the process that stimulus at a critical period of development has lifelong effects. The fact that low birth weight links to the risk of elevated blood pressures in adult life is well known. This study aims to examine whether this link is evident in the newborn by investigating the relationship of the intrauterine growth indices and neonatal blood pressure(BP). Methods : We studied 127 neonates who were born at Ewha Womans' Hospital and their mothers enrolled our cohort study during pregnancy. Data on the mothers and details of the birth records were tracked and collected from medical charts. Neonatal BP was measured within 24 hours after birth. Results : Neonatal SBP was positively correlated to intrauterine growth indices; birth weight(BW)(r=0.4), head circumference(HC)(r=0.4), and birth height(r=0.3). However, an inverse relationship existed, between HC/BW ratio and neonatal SBP(r=-0.4). After adjusting for the baby's sex, maternal BP, and gestational age, neonatal SBP still associated with intrauterine growth indices. SBP was 7 mmHg higher in the highest BW group(${\geq}90percentiles$) compared to the lowest group(<10 percentiles). On the other hand, SBP was 17 mmHg lower in the highest HC/BW group(${\geq}90percentiles$) compared in the lowest group(<10 percentiles). Conclusion : This study could not find the evidence that intrauterine growth retardation affect on elevated neonatal BP. It suggests that the initiating events of BP programming may occur during postnatal growth period. To identify the critical starting period that intrauterine growth retardation leads to elevated BP, a study tracking BP changes from birth to childhood is required.

• Nutrition Research and Practice
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• v.15 no.2
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• pp.160-172
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• 2021

BACKGROUND/OBJECTIVES: Nutritional status and food intake during pregnancy and lactation can affect fetal programming. In the current metabolic syndrome epidemic, high-fructose diets have been strongly implicated. This study investigated the effect of maternal high-fructose intake during pregnancy and lactation on the development of metabolic syndrome in adult offspring. SUBJECTS/METHODS: Drinking water with or without 20% fructose was administered to female C57BL/6J mice over the course of their pregnancy and lactation periods. After weaning, pups ate regular chow. Accu-Chek Performa was used to measure glucose levels, and a tail-cuff method was used to examine systolic blood pressure. Animals were sacrificed at 7 months, their livers were excised, and sections were stained with Oil Red O and hematoxylin and eosin (H&E) staining. Kidneys were collected for gene expression analysis using quantitative real-time Polymerase chain reaction. RESULTS: Adult offspring exposed to maternal high-fructose intake during pregnancy and lactation presented with heavier body weights, fattier livers, and broader areas under the curve in glucose tolerance test values than control offspring. Serum levels of alanine aminotransferase, aspartate aminotransferase, glucose, triglycerides, and total cholesterol and systolic blood pressure in the maternal high-fructose group were higher than that in controls. However, there were no significant differences in mRNA expressions of renin-angiotensin-aldosterone system genes and sodium transporter genes. CONCLUSIONS: These results suggest that maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome with hyperglycemia, hypertension, and dyslipidemia in adult offspring.