Abstract 16195: A Novel Differential Role of Apolipoprotein C-I on the Expression of Large HDL and Triglycerides in Infants at Birth and Follow-Up Compared With Their Parents
At birth, HDL is the major lipoprotein class and the largest (> 10 nm) HDL subclass, H5C, is elevated in 20 % of infants, absent in another 20% with the rest intermediate. In utero, apolipoprotein C-I (apoC-I), a small, basic protein, is carried exclusively on HDL, where it increases LCAT but inhibits CETP and the HDL receptor, promoting the formation of H5C. Later in life, ApoC-I is also associated with VLDL, where it inhibits the binding of apolipoprotein E on triglyceride-rich lipoproteins to the LDL receptor.
Objective: To determine the effect of apoC-I on H5C and triglycerides (TG) in infants at birth compared with enterally-fed infants at follow-up (FU) and their parents.
Methods: Families (N = 103) were ascertained through pregnant women (N=103) at the Greater Baltimore Medical Center. Infants at birth (N = 103) and FU at 2-3 months of age (N = 85) and fathers (N = 73) were studied. Lipids, lipoproteins and their subclasses were determined by NMR spectroscopy. Correlations of lipid-related parameters were calculated using Spearman rank correlations.
Results: ApoC-I was strongly and positively correlated with H5C both in infants at birth and FU (table) but there was no correlation with TG. In contrast, the level of TG in both parents was highly correlated with apoC-I; the correlation of apoC-I with H5C was negative but NS (table).
Conclusion: These data indicate that apoC-I has a different effect on the expression of H5C and TG early compared to later in life. These effects are similar at birth and FU in enterally fed infants, indicating that H5C and apoC-I may play a distinct and potentially important role in lipoprotein metabolism early in life. It remains to be determined whether infants with elevated H5C and higher apoC-I manifest different pathophysiological characteristics later in life than infants with little H5C and low apoC-I levels.
- © 2011 by American Heart Association, Inc.