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Metabolomics; Gestational weight gain; Offspring; Newborn; Umbilical cord

Introduction

It has been hypothesized that the unfavorable intrauterine environment may sustain programmed adaptations in fetal development until ectopic life, resulting in a phenotype predisposed to cardiovascular disease [1]. An example of an unfavorable intrauterine environment is fetal overnutrition, defined as fetal exposure to excess maternal fuel due to maternal obesity, gestational diabetes (GD), or excessive gestational weight gain (GWG) [2]. Numerous epidemiological, clinical, and animal model studies have shown that maternal prenatal obesity and high-fat diet intake are associated with obesity, hypertension, hyperglycemia and insulin resistance, hyperlipidemia, non-alcoholic fatty liver disease, etc [3]. It strongly suggests that it is associated with cardiometabolic disease in offspring [4].

A number of studies suggest that the umbilical cord plasma metabolite profile (obtained from the fetal response to in utero exposure) may serve as a long-term biomarker of metabolic disease risk during childhood. Therefore, although there is increasing interest in investigating the cord blood metabolomic profile of mother-infant pairs, studies conducted to date have yielded inconsistent results [5]. Perng et al. Energy production and DNA/RNA turnover pathway metabolites and branched-chain amino acids (BCAAs) in cord blood are associated with increased neonatal size, a known risk factor for poor cardiovascular health later in life and that BCAAs and androgens are involved. Hormone patterns were higher in obese than in lean school-age children (ages 6-10). In addition, higher factor scores for these patterns correlated with continuous measures of total and central fat percentage and higher her HOMA-IR and other cardiometabolic biomarkers [6]. Cord blood BCAAs and ketone body metabolites have been found to be positively correlated with neonatal obesity. Linked umbilical cord plasma metabolites with longitudinal BMI trajectories in 946 children from birth to 18 years of age [7].

Discussion

Maternal GWG during pregnancy is an important factor in fetal growth and development and can have a significant impact on subsequent offspring’s metabolic health [8]. The aim of our study was to investigate the metabolic profiles of children at birth, 6 months and 12 months of age and to analyze them in terms of maternal GWG. Previous studies have explored the relationship between offspring’s metabolic profile and maternal metabolic status, but both regression and multivariate PLS-DA models have been used with adaptations to confounders and is the first study to analyze profiles in terms of maternal GWG [9]. Considering both maternal and child confounders allowed for more accurate association detection and reduced false positives. Many metabolic associations were identified in our combinatorial analysis, most of which were present in either tertile or linear regression analyses, leading to complex nonlinearities likely modulated by many external factors. Suggests a relationship indeed, only at birth did the three tertiles follow a progressive trend from 1 to 2 and then to tertiary, but at 6 and 12 months the other tertiles there seems to have been a distinction between the upper and lower tertiles with respect. Interpretation of these results is by no means straightforward, but the scoreplot suggests that several metabolic alterations that may have been regulated by the mother’s GWG occurred during the first 12 months of life [10].

Conclusions

Overall, the mechanisms underlying the association between maternal weight gain and the infant’s metabolic profile are not well understood, but increased maternal weight gain leads to changes in placental function and metabolism that in turn affect the infant’s It has been hypothesized that it may affect the metabolism of fetuses and infants. We identified several metabolites that were linearly or nonlinearly associated with maternal weight gain and tertiles. This may help identify metabolic pathways and clusters involved in long-term effects. Our metabolite accumulation analysis. We suggest that studying hypoxic metabolism, ketogenesis, and ammonia-related pathways may help to understand this link. The presence of high-amino shortchain fatty acid derivatives, methylamines, and choline-containing compounds in all of our major metabolic pathways suggests a relevant role for nitrogen metabolism in this interaction network. Further studies are needed to elucidate the mechanisms by which maternal GWG regulates these changes in the offspring’s metabolome and their long-term consequences later in life. Our current knowledge makes it very difficult to translate these metabolic insights into clinical routine, but further research is required to use more individualized feeding and growth monitoring interventions to reduce risk. May help identify certain infants.

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