Abstracts

Longitudinal change of intrahepatocellular lipid in early infancy

Presented at the Neonatal Society 2011 Autumn Meeting.

Gale C, Jeffries S, Parkinson JRC, Logan K, Santhakumaran S, Hyde MJ, Durighel G, Thomas EL, Bell JD, Modi N

Imperial College London, UK

Background: Intrahepatocellular lipid (IHCL) represents a potentially important fat reserve in early infancy, but in later life excess is closely associated with insulin resistance. Our group has shown increased IHCL in ex-preterm infants at term equivalent age and as young adults (1,2), and a direct relationship between maternal BMI and infant IHCL in term infants (3). In this study we aim to describe the changes in IHCL during early infancy in healthy, term babies. Research Ethics Committee approval has been granted (10/H0713/5).

Methods: Healthy, term (37+0 to 41+6 weeks+days), appropriate weight for gestational age infants (WHO Child Growth Standards) of non-diabetic mothers, were recruited from the postnatal ward at Chelsea and Westminster Hospital. Longitudinal scans were performed, after birth and at 2-3 months, in natural sleep, in a supine position. Heart rate and oxygen saturation were monitored continuously and a neonatal paediatrician was present throughout the procedure. Proton magnetic resonance spectra were acquired on a Phillips 1.5 T system as previously described (1) with IHCL values adjusted for T1 and T2 effects and using hepatic water as an internal standard. Results are presented as IHCL CH2/water. Data were analysed using SPSS 19. IHCL is non-normally distributed and includes zero values, therefore the difference in paired IHCL data was examined using related samples Wilcoxon signed rank test, and for multiple regression analyses a constant calculated to minimise skew (0.005) was added, and loge transform taken. Loge(IHCL + 0.005) is denoted as LnIHCL.

Results: Thirty-three infants (21 male), mean (SD) birthweight 3.395kg (0.406), birthweight SDS -0.11 (0.83), gestational age 40+1 (1+1) and maternal BMI 23.5 (4.2), underwent longitudinal scans. Population characteristics at scans and IHCL values, are represented in the table below:

Longitudinal change of intrahepatocellular lipid in early infancy

In comparison with the first scan, IHCL is increased at the second scan (p=0.001). Multivariate analyses revealed no significant effect of feeding mode or maternal BMI on second scan IHCL after adjusting for first scan IHCL.

Conclusion: The increasing IHCL we document in early infancy, to values greater than those seen in healthy lean adults (1,4), raises intriguing questions about hepatic lipid handling in infancy. This may represent an evolutionary response to store energy for use during weaning or reflect immaturity of lipid metabolism in early life. Further work must concentrate on identifying factors influencing IHCL accretion, determining the natural history of IHCL in childhood and elucidating the relationship between early life IHCL and metabolic health.

Corresponding author: christopher.gale@imperial.ac.uk

References
1. Thomas EL, et al. Arch Dis Child Fetal Neonatal Ed. 2008 Sep;93(5):F382-3.
2. Thomas EL, et al. Pediatr Res. 2011 Jul 18.
3. Modi N, et al. Pediatr Res. 2011 Sep;70(3):287-91.
4. Thomas EL, et al. Obesity (Silver Spring). 2011 Jun 9.

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