Abstract

Children born with IUGR develop features of the metabolic syndrome and exhibit deranged markers of hepatorenal physiology. Metabolic and hepatorenal biochemistry and the rs9939609 FTO polymorphism were investigated in prepubertal children born with IUGR. Ninety-eight prepubertal children (46 IUGR and 52 AGA), subdivided in <5 years and >5 years old groups were included. Anthropometry; creatinine, eGFR, urea, AST, ALT, triglycerides, uric acid, total cholesterol, HDL-c, LDL-c, glucose, C-peptide, insulin and glucagon z-scores; HOMA-IR; leptin and adiponectin concentrations; rs9939609 FTO polymorphism frequency were measured. In males, weight and ALT were higher and adiponectin was lower, in IUGR < 5 years; C-peptide, insulin and leptin were higher in IUGR > 5 years; C-peptide was higher in all IUGR, than the respective AGA. In females, creatinine and triglycerides were higher in IUGR < 5 years old; creatinine was higher and eGFR was lower in all IUGR, than the respective AGA. In males and females, creatinine was higher in all IUGR, than the respective AGA; C-peptide, insulin and HOMA-IR were lower, and AST was higher in IUGR < 5 than in IUGR > 5 years old. FTO rs9939609 frequency did not differ between IUGR and AGA. In conclusion prepubertal males born with IUGR increased weight, insulin and leptin and decreased adiponectin, as compared to males born AGA, emerge as early metabolic syndrome characteristics. The concentrations of these hormones do not differ between prepubertal males and females born with IUGR. Weight control, healthy nutrition and physical exercise should be recommended to these children. The deranged renal (particularly evident in females below the age of 5) and liver biochemistry in prepubertal children born with IUGR suggests that hepatorenal derangements might commence in utero. Regular checkup of biochemical and lipid profile is recommended for all children born with IUGR.

Highlights

  • In intrauterine growth restriction (IUGR) fetus fails to achieve its growth potential due to genetic or environmental factors in utero[1]

  • In subjects born with IUGR mean weight and body mass index (BMI) z-scores were significantly higher in males than in females (p < 0.05) (Table 3)

  • We found that birth weight and length were lower in all subjects born with IUGR compared to those born appropriate for gestational age (AGA), as expected[1,4]

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Summary

Introduction

In intrauterine growth restriction (IUGR) fetus fails to achieve its growth potential due to genetic or environmental factors in utero[1]. The term small for gestational age (SGA) refers to an infant whose birth weight is below the 10th centile for the appropriate gestational age[2]. This clinical problem affects approximately 8% of pregnancies and is associated with perinatal mortality and morbidity[4]. Intrauterine growth restriction, as originally been suggested in the “thrifty phenotype” hypothesis by Barker et al, has been causally associated with the development of metabolic syndrome in adulthood and with long-term metabolic sequelae such as obesity, impaired glucose tolerance, diabetes mellitus type 2 (T2DM), hypertension, dyslipidemia, cardiovascular disease and polycystic ovary syndrome (PCOS)[7,8,9,10,11]. Girls born with low birth weight, followed by postnatal catch up growth, exhibit increased visceral fat and insulin resistance in pre-school age[11]. The possible association of the rs9939609 polymorphism of FTO gene with the development of obesity was investigated

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