Cord blood concentrations of leptin, zinc-α2-glycoprotein, and adiponectin, and adiposity gain during the first 3 mo of life

Euclydes, Veronica Luiza Vale; Castro, Natália; Lima, L R A Vaz de; Brito, Cyro Alves de; Ribeiro, L. V.; Simoes, F.; Requena, Guaraci; Luzia, Liânia Alves; Rondó, Patrícia Helen de Carvalho

doi:10.1016/j.nut.2018.02.012

Cited by 11 publications

(9 citation statements)

References 40 publications

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“…In the study by Näf et al [78] ZAG in cord blood was positively correlated with fat-free mass, birth weight and gestational age at delivery. On the other hand, Euclydes et al [79] examined the relationship between ZAG and fat mass in infancy. ZAG concentrations in cord blood were inversely proportional to weight gain in girls.…”

Section: Impact Of Zag On Lipid Metabolismmentioning

confidence: 99%

Zinc and the Innovative Zinc-α2-Glycoprotein Adipokine Play an Important Role in Lipid Metabolism: A Critical Review

2021

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Numerous studies indicate that zinc and the new zinc-related adipokine, zinc-α2-glycoprotein (ZAG), are involved in lipid metabolism. Excess body fat lowers blood concentrations of Zn and ZAG, leading not only to the development of obesity but also to other components of the metabolic syndrome. Zinc homeostasis disorders in the body negatively affect the lipid profile and cytokine secretion. Zinc appears to be a very important ZAG homeostasis regulator. The physiological effects of ZAG are related to lipid metabolism, but studies show that ZAG also affects glucose metabolism and is linked to insulin resistance. ZAG has a zinc binding site in its structure, which may indicate that ZAG mediates the effect of zinc on lipid metabolism. The review aimed to verify the available studies on the effects of zinc and ZAG on lipid metabolism. A literature review within the scope of this research area was conducted using articles available in PubMed (including MEDLINE), Web of Science and Cochrane Library databases. An analysis of available studies has shown that zinc improves hepatic lipid metabolism and has an impact on the lipid profile. Numerous studies have found that zinc supplementation in overweight individuals significantly reduced blood levels of total cholesterol, LDL (Low-density lipoprotein)cholesterol and triglycerides, potentially reducing cardiovascular morbidity and mortality. Some results also indicate that it increases HDL-C (High-density lipoprotein) cholesterol levels. ZAG has been shown to play a significant role in reducing obesity and improving insulin sensitivity, both in experimental animal model studies and in human studies. Furthermore, ZAG at physiologically relevant concentrations increases the release of adiponectin from human adipocytes. In addition, ZAG has been shown to inhibit in vitro leptin production. Further studies are needed to provide more data on the role of zinc and zinc-α2-glycoprotein.

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Section: Impact Of Zag On Lipid Metabolismmentioning

confidence: 99%

Zinc and the Innovative Zinc-α2-Glycoprotein Adipokine Play an Important Role in Lipid Metabolism: A Critical Review

2021

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“…Insulin is secreted by pancreatic β-cells and is primarily responsible for glucose homeostasis [69]. All three cytokines have implications for energy balance and metabolism as previous studies of cord blood concentrations reported associations with adiposity at birth or in early life [70][71][72][73]. Biomarker concentrations were quantified using commercially available assays (Meso Scale Discov-ery® Multi-Spot Assay System® for leptin and insulin; R&D Systems™ Human HMW Adiponectin/Acrp30 Quantikine ELISA Kit for adiponectin).…”

Section: Birth Outcome and Biomarker Assessmentmentioning

confidence: 99%

Predictors and reproducibility of urinary organophosphate ester metabolite concentrations during pregnancy and associations with birth outcomes in an urban population

et al. 2020

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Background Organophosphate esters (OPEs) are synthetic chemicals used as flame retardants and plasticizers in a variety of goods. Despite ubiquitous human exposures and laboratory evidence that prenatal OPE exposures may disrupt offspring metabolism, perinatal studies of OPE health effects are limited. The objectives of this study were to: 1) Determine predictors and reproducibility of urinary OPE biomarker concentrations during pregnancy, and 2) Estimate the relation of prenatal OPE exposures with birth outcomes and cord blood adipokine and insulin concentrations. Methods We analyzed five OPE metabolites in urine samples collected at up to three visits during pregnancy from 90 women enrolled in the ORigins of Child Health And Resilience in Development (ORCHARD) pregnancy cohort in Baltimore, MD from 2017 to 2019. To quantify the variability of metabolite concentrations during pregnancy, we calculated intraclass correlation coefficients (ICCs) for each metabolite using mixed effects regression models. Using self-reported questionnaire data collected during gestation, we assessed possible sociodemographic and environmental/behavioral predictors of each OPE metabolite using generalized estimating equations to account for repeated exposure measures. We ascertained birth outcomes of 76 offspring from medical records, including weight-for-gestational age, length, ponderal index, and gestational age. In a subset of 37 infants, we measured cord blood concentrations of leptin, adiponectin, and insulin. To account for repeated exposure measures, we used linear structural equation models to assess the relations of standard deviation (SD) increases in prenatal OPE metabolite factor scores with continuous birth outcomes and cord blood biomarker concentrations. Results ICCs ranged from 0.09 for isopropylphenyl-phenyl phosphate (ip-PPP) to 0.59 for bis(1,3-dichloro-2-propyl) phosphate (BDCIPP). We observed little consistency in environmental or behavioral predictors of OPE exposures, although concentrations were generally lower for samples collected in the afternoon compared to morning and winter compared to other seasons. In adjusted analyses, a SD increase in BDCIPP concentration was associated with a 0.06 g/cm3 (95% CI: 0.00, 0.12) greater ponderal index. A SD increase in BDCIPP was associated with a 0.37 (95% CI: − 0.62, − 0.13) SD lower insulin concentration and 0.24 (95% CI: − 0.39, − 0.08) SD lower leptin concentration. Other OPEs were not associated with infant outcomes. Conclusions These findings suggest some OPEs may be metabolic disruptors warranting investigation in larger studies.

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“…The degree of cord leptin is associated not only with the birth weight, but also with postnatal body weight gain [ 45 , 46 , 49 , 50 , 51 ]. While high cord leptin mediates a gradual gain of infant body weight and adiposity [ 45 , 51 ], low neonatal leptin results in rapid body weight gain during the early postnatal period, making low neonatal leptin a strong risk factor for childhood obesity [ 50 ]. This negative correlation between cord leptin and infant body weight gain is sustained in early childhood, up to the age of 4, then switches to a positive relationship in later childhood and adolescence [ 44 , 46 ].…”

Section: Early Leptin For Future Cardiometabolic Outputmentioning

confidence: 99%

“…The degree of cord leptin is associated not only with the birth weight, but also with postnatal body weight gain [45,46,[49][50][51]. While high cord leptin mediates a gradual gain of infant body weight and adiposity [45,51], low neonatal leptin results in rapid body weight gain during the early postnatal period, making low neonatal leptin a strong risk factor for childhood obesity [50].…”

Section: Maternal and Cord Leptin During Gestationmentioning

confidence: 99%

Temporal Leptin to Determine Cardiovascular and Metabolic Fate throughout the Life

2020

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Leptin links peripheral adiposity and the central nervous system (CNS) to regulate cardiometabolic physiology. Within the CNS, leptin receptor-expressing cells are a counterpart to circulating leptin, and leptin receptor-mediated neural networks modulate the output of neuroendocrine and sympathetic nervous activity to balance cardiometabolic homeostasis. Therefore, disrupted CNS leptin signaling is directly implicated in the development of metabolic diseases, such as hypertension, obesity, and type 2 diabetes. Independently, maternal leptin also plays a central role in the development and growth of the infant during gestation. Accumulating evidence points to the dynamic maternal leptin environment as a predictor of cardiometabolic fate in their offspring as it is directly associated with infant metabolic parameters at birth. In postnatal life, the degree of serum leptin is representative of the level of body adiposity/weight, a driving factor for cardiometabolic alterations, and therefore, the levels of blood leptin through the CNS mechanism, in a large part, are a strong determinant for future cardiometabolic fate. The current review focuses on highlighting and discussing recent updates for temporal dissection of leptin-associated programing of future cardiometabolic fate throughout the entire life.

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Cord blood concentrations of leptin, zinc-α2-glycoprotein, and adiponectin, and adiposity gain during the first 3 mo of life

Cited by 11 publications

References 40 publications

Zinc and the Innovative Zinc-α2-Glycoprotein Adipokine Play an Important Role in Lipid Metabolism: A Critical Review

Zinc and the Innovative Zinc-α2-Glycoprotein Adipokine Play an Important Role in Lipid Metabolism: A Critical Review

Predictors and reproducibility of urinary organophosphate ester metabolite concentrations during pregnancy and associations with birth outcomes in an urban population

Temporal Leptin to Determine Cardiovascular and Metabolic Fate throughout the Life

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