Role of lipidomics in assessing the functional lipid composition in breast milk.

Breast milk is the ideal source of nutrients for infants in early life. Lipids represent 2-5% of the total breast milk composition and are a major energy source providing 50% of an infant's energy intake. Functional lipids are an emerging class of lipids in breast milk mediating several different biological functions, health, and developmental outcome. Lipidomics is an emerging field that studies the structure and function of lipidome. It provides the ability to identify new signaling molecules, mechanisms underlying physiological activities, and possible biomarkers for early diagnosis and prognosis of diseases, thus laying the foundation for individualized, targeted, and precise nutritional management strategies. This emerging technique can be useful to study the major role of functional lipids in breast milk in several dimensions. Functional lipids are consumed with daily food intake; however, they have physiological benefits reported to reduce the risk of disease. Functional lipids are a new area of interest in lipidomics, but very little is known of the functional lipidome in human breast milk. In this review, we focus on the role of lipidomics in assessing functional lipid composition in breast milk and how lipid bioinformatics, a newly emerging branch in this field, can help to determine the mechanisms by which breast milk affects newborn health.

Breast Milk from Non-Obese Women with a High Omega-6 to Omega-3 Fatty Acid Ratio, but Not from Women with Obesity, Increases Lipogenic Gene Expression in 3T3-L1 Preadipocytes, Suggesting Adipocyte Dysfunction.

Maternal body mass index is associated with breast milk (BM) fatty acid composition. This study investigated the effects of BM omega (n)-6:n-3 polyunsaturated fatty acids (PUFAs) from non-obese women and women with obesity on the process of adipogenesis in 3T3-L1 preadipocytes. BM samples were collected from non-obese women (BMNO) and women with obesity (BMO) at one month postpartum. The fatty acid composition was measured, and BMNO and BMO groups with the lowest (Q1) and highest (Q4) quartiles of n-6:n-3 PUFA ratios were identified. 3T3-L1 preadipocytes were differentiated in the presence or absence of BM. Lipid accumulation and the expression of genes involved in lipogenesis and lipolysis were measured. Treatment with BMNO containing high (vs. low) n-6:n-3 PUFA ratios significantly increased the mRNA expression of lipogenic genes (acetyl-CoA carboxylase, fatty acid synthase, and stearoyl-CoA desaturase); however, there was no effect when cells were treated with BMO (with either low or high n-6:n-3 PUFA ratios). Treatment with BMO (high n-6:n-3 PUFA ratio) caused larger lipid droplets. Our findings demonstrated that BMNO with a high n-6:n-3 PUFA ratio was associated with a higher expression of lipogenic genes, while BMO with a high n-6:n-3 PUFA ratio showed larger lipid droplets, suggesting adipocyte dysfunction. These findings may have implications in the BM-mediated programming of childhood obesity.

The impact of maternal obesity and breast milk inflammation on developmental programming of infant growth.

BACKGROUND: Little is known about how maternal obesity impacts breast milk (BM) composition and how BM composition may impact growth. We sought to determine the role of maternal body mass index (BMI) on BM inflammatory and oxidative stress markers and to delineate the role of these BM markers on infant growth. METHODS: This was a secondary analysis of 40 mother-infant dyads. We first assessed the association between maternal BMI and BM marker (omega-6:omega-3 polyunsaturated fatty acid ratio (n-6:n-3 PUFA), leptin, interleukin (IL)-8, IL-6, IL-1ß and malondialdehyde (MDA)) concentration at one (V1) and four (V4) months postpartum. We then examined the association between BM markers on infant growth trajectory from birth to seven months. RESULTS: Higher maternal BMI was associated with higher BM n-6:n-3 PUFA (V1 ß = 0.12, 95% CI 0.01, 0.2; V4 ß = 0.13, 95% CI 0.01, 0.3) and leptin (V1 ß = 107, 95% CI 29, 184; V4 ß = 254, 95% CI 105, 403) concentrations. Infants exposed to high BM n-6:n-3 PUFA had higher BMI z-scores over time (p = 0.01). Higher BM leptin was associated with lower infant percent fat mass at V4 (ß = -9, 95% CI -17, -0.6). Infants exposed to high BM IL-8, IL-6, or IL-1ß had higher weight z-scores over time (IL-8 p < 0.001; IL-6 p < 0.001; IL-1ß p = 0.02). There was no association between BM MDA and maternal BMI or infant growth. CONCLUSIONS: Higher maternal BMI is associated with higher BM n-6:n-3 PUFA and leptin concentrations. In addition, higher BM n-6:n-3 PUFA and inflammatory cytokines were associated with accelerated weight gain in infancy.

Father's Lifetime Socioeconomic Status, Small for Gestational Age Infants, and Infant Mortality: A Population-Based Study.

Objective: To ascertain the association between father's lifetime socioeconomic status (SES) and rates of small for gestational age (SGA, defined as weight for gestational age <10th percentile) and infant mortality (defined as <365 days). Methods: The study sample was limited to the singleton births of African American (n=8,331), non-Latina White (n=18,200), and Latina (n=2,637) women. Stratified and multilevel, multivariable logistic regression analyses were conducted on the Illinois transgenerational dataset of infants (1989-1991) and their Chicago-born parents (1956-1976) with appended US census income data (n=29,168). The median family income of father's census tract residence during childhood and parenthood were used to assess lifetime SES. Results: Births (n=8,113) to fathers with a lifetime low SES had a SGA rate of 13.3% compared with 6.6% for those (n=10,329) born to fathers with a lifetime high SES, RR = 1.97 (1.79, 2.17). The infant mortality rate of births to fathers with a lifetime low SES exceeded that of infant mortality rate of births to fathers with a lifetime high SES: 13/1,000 vs 5/1,000, respectively; RR = 2.71 (1.94, 3.77). The adjusted (controlling for mother's age, education, marital status, and race/ethnicity) OR of SGA for fathers with childhood, parenthood, and lifetime low (vs high) SES were 1.15 (1.01, 1.31), 1.13 (1.02, 1.26), and 1.19 (1.05, 1.34), respectively. The adjusted OR of infant mortality for births to fathers with childhood, parenthood, and lifetime low (vs high) SES were 1.14 (.78, 1.67), 1.40 (.90, 2.18), and 1.31 (.90, 1.92), respectively. Conclusions: Low paternal socioeconomic status is a previously unrecognized determinant of SGA birth regardless of mother's demographic status.