Unadjusted and adjusted model of linear regression between <i>apoB/apoA1 ratio</i> levels (dependent variable) and independent variables.

Unadjusted and adjusted model of linear regression between apoB/apoA1 ratio levels (dependent variable) and independent variables.</p

Descriptive data of men and women with birth weight data in the LifeGene cohort.

Descriptive data of men and women with birth weight data in the LifeGene cohort.</p

General linear regression model of the association between birth weight (adjusted for confounders and covariates) and <i>apoA1 levels</i> (dependent variable).

General linear regression model of the association between birth weight (adjusted for confounders and covariates) and apoA1 levels (dependent variable).</p

Unadjusted and adjusted model of linear regression between <i>total cholesterol</i> (dependent variable) and independent variables.

Unadjusted and adjusted model of linear regression between total cholesterol (dependent variable) and independent variables.</p

Unadjusted and adjusted model of linear regression between log-transformed <i>triglyceride levels</i> (dependent variable) and independent variables.

Unadjusted and adjusted model of linear regression between log-transformed triglyceride levels (dependent variable) and independent variables.</p

Flow chart of the study sample from the LifeGene study cohort (n = 10093).

Flow chart of the study sample from the LifeGene study cohort (n = 10093).</p

Generalized linear regression model of association between birth weight (adjusted for confounders and covariates) and <i>apoB levels</i> (dependent variable).

Generalized linear regression model of association between birth weight (adjusted for confounders and covariates) and apoB levels (dependent variable).</p

S1 Data -

BackgroundEarly life factors may predict cardiovascular disease (CVD), but the pathways are still unclear. There is emerging evidence of an association of early life factors with apolipoproteins, which are linked to CVD. The study objective was to assess the associations between birth variables and adult apolipoproteins (apoA1 and apoB, and their ratio) in a population-based cohort.MethodsThe LifeGene Study is a prospective cohort comprising index participants randomly sampled from the general population. Blood samples were collected between 2009 and 2016. In this sub-study, we used birth variables, obtained from a national registry for all participants born 1973 or later, including birth weight and gestational age, while adult CVD risk factors included age, sex, body mass index (BMI), lipids, and smoking history. We employed univariate and multivariate general linear regression to explore associations between birth variables, lipid levels and other adult CVD risk factors. The outcomes included non-fasting apoA1 and apoB and their ratio, as well as total cholesterol and triglycerides. A total of 10,093 participants with both birth information and lipoprotein levels at screening were included. Of these, nearly 42.5% were men (n = 4292) and 57.5% were women (n = 5801).ResultsThe mean (standard deviation) age of men was 30.2 (5.7) years, and for women 28.9 (5.8) years. There was an increase of 0.022 g/L in apoA1 levels per 1 kg increase in birth weight (p = 0.005) after adjusting for age, sex, BMI, gestational age, and smoking history. Similarly, there was a decrease of 0.023 g/L in apoB levels per 1 kg increase in birth weight (p-0.067 (-0.114, -0.021); p-value 0.005).ConclusionsLower birth weight was associated with an adverse adult apolipoprotein pattern, i.e., a higher apoB/apoA1 ratio, indicating increased risk of future CVD manifestations. The study highlights the need of preconception care and pregnancy interventions that aim at improving maternal and child outcomes with long-term impacts for prevention of cardiovascular disease by influencing lipid levels.</div

Surface plasmon resonance (SPR) sensorgrams of S-MB or MB binding to immobilized Cys-S-MB or Cys-MB.

<p>S-MB and MB, each with a cysteine added to its N-terminus, were attached to the thiol Biacore chip as described in the text. Solutions of S-MB or MB in HBS-EP buffer (i.e., 10 mM Hepes, pH 7.4, 150 mM NaCl, 3 mM EDTA, 0.005% surfactant P20) were then flowed over the respective chip-linked peptides. Typical SPR responses [Y-axis indicates the relative amount of binding in arbitrary response units (RU)] are shown for either 1 µg S-MB/ml buffer to chipped Cys-S-MB (black line) or chipped Cys-MB (green line), or with 1 µg MB/ml buffer to chipped Cys-S-MB (red line) or Cys-MB (blue line). Relative peptide affinities are: S-MB to S-MB ≫ S-MB to MB∼ MB to S-MB ∼ MB to MB.</p

Mean association and dissociation kinetic rate constants (k_on, k_off) and equilibrium dissociation constants (KD), calculated from surface plasmon resonance (SPR) measurements for aqueous Mini-B (MB) and Super Mini-B (S-MB) flowing past chip-linked Cys-MB and Cys-S-MB monolayers^a.

a<p>MB and S-MB in running buffer (10 mM HEPES, 150 mM NaCl, 3 mM EDTA, 0.005% Surfactant P20, pH 7.4) were flowed past monolayers of N-terminal Cys-MB or N-terminal Cys-S-MB, linked via their respective N-terminal thiol groups to CSM sensor chips in a Biacore 3000 system (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0008672#s2" target="_blank">Methods</a>).</p><p>Mean kinetic rate constants (k_on, k_off) and equilibrium dissociation constants (KD = k_off/k_on) were determined from curve fitting analyses of SPR results at 1 µg peptide/ml buffer.</p