A comparative analyses of lipid ratios representing desaturase enzyme activity between preterm and term infants within the first ten weeks of life
Background: Desaturase enzymes play a key role in several pathways including biosynthesis of poly- and mono- unsaturated fatty acids (PUFAs, MUFA). In preterm infants, desaturase enzyme activity (DA) may be a rate-limiting step in maintaining PUFAs levels during this critical developmental window and impact on long term metabolic health. The study tested the hypothesis that DA is altered in preterm infants compared to term infants in early life and may be a marker of risk or contribute to later alterations in metabolic health. Methods: Lipidomic analyses were conducted using blood samples from two established UK-based cohorts, involving very preterm (n = 105) and term (n = 259) infants. Blood samples were taken from term infants at birth, two and six weeks and from preterm infants when established on enteral feeds and at term corrected age. DA of the 2 groups of infants were estimated indirectly from product/precursor lipids ratios of phosphatidylcholine (PC) and triglycerides (TG) species and reported according to their postmenstrual and postnatal ages. Results: There were changes in lipid ratios representing desaturase enzyme activity in preterm infants in the first weeks of life with higher delta 6 desaturases (D6D) triglyceride (TG) indices but significantly lower delta 9 desaturase (D9D) and D6D(PC) indices. In comparison to term infants, preterm have lower delta 5 desaturase (D5D) but higher D6D indices at all postnatal ages. Although point levels of desaturase indices were different, trajectories of changes in these indices over time were similar in preterm and term infants. Conclusions: This study findings suggest the patterns of desaturase indices in preterm infants differ from that of term infants but their trajectories of change in the first 10 weeks of life were similar. These differences of DA if they persist in later life could contribute to the mechanism of diseases in preterm adulthood and warrant further investigations.
Acknowledgements: We wish to thank the research nurses, Lynn Thomson, Ann-Marie Wardell, Suzanne Smith and Karen Forbes for recruitment and sample collection. The families of all those who participated in the studies and the clinical teams in the antenatal clinics, postnatal wards and neonatal unit at Cambridge University Hospital NHS Trust for all their support with the study. We want to thank the financial support of the Biotechnology and Biological Sciences Research Council (BB/P028195/1) for SGS and the NIHR Cambridge Biomedical Research Centre (146281) for Albert Koulman.
Funder: Jardine Foundation
Funder: Cambridge Trust
Funder: Universiti Sains Islam Malaysia; doi: http://dx.doi.org/10.13039/501100010187
Funder: The National Institute for Health Research Cambridge Biomedical Research Centre.
Mothercare Charitable Foundation (RG54608)
European Union Framework 5 (QLK4- 1999?01422)
Newlife Foundation for Disabled Children (07/20)