Maternal Zinc Research Articles

Plasma zinc levels in Ecuadorian mothers of infants with nonsyndromic cleft lip with or without cleft palate: A case series.

Previous studies have reported an association between maternal zinc deficiency and increased risk of nonsyndromic cleft lip with or without cleft palate (NSCL/P) in offspring. A high prevalence of zinc deficiency and a high prevalence of NSCL/P have been reported in Ecuador. We postulated that mothers of infants with NSCL/P may have lower serum zinc levels than women from the general population. A case series study was conducted from November 2013 to July 2016. Thirty-five healthy mothers of infants with NSCL/P were selected during surgical missions conducted by Operación Sonrisa Ecuador. A single blood sample along with pertinent medical history was collected during personal interviews after 3.6 months postpartum. The prevalence of plasma zinc concentration (PZn) deficiency among the participants was determined and analyzed along with the prevalence of PZn deficiency in Ecuadorian women of reproductive age from the general population. The mean PZn was 11.47 µmol/dm3 . The prevalence of PZn deficiency among the participants was 31.4% (95% CI: 17.1-48.6) and differed significantly from the prevalence of zinc deficiency observed among women from the general population (G2 = 8.66; p < .05). The results showed that the prevalence of PZn deficiency is lower in a cohort of healthy mothers of infants with NSCL/P than in women from the general population in Ecuador. More studies are required to confirm these findings and evaluate other factors related to NSCL/P pathophysiology in the Ecuadorian population.

Zinc deficiency as a mediator of toxic effects of alcohol abuse.

To review data on the role of ethanol-induced alteration of Zn homeostasis in mediation of adverse effects of alcohol abuse. The scholarly published articles on the association between Zn metabolism and alcohol-associated disorders (liver, brain, lung, gut dysfunction, and fetal alcohol syndrome) have been reviewed. It is demonstrated that alcohol-induced modulation of zinc transporters results in decreased Zn levels in lungs, liver, gut, and brain. Zn deficiency in the gut results in increased gut permeability, ultimately leading to endotoxemia and systemic inflammation. Similarly, Zn deficiency in lung epithelia and alveolar macrophages decreases lung barrier function resulting in respiratory distress syndrome. In turn, increased endotoxemia significantly contributes to proinflammatory state in alcoholic liver disease. Finally, impaired gut and liver functions may play a significant role in alcoholic brain damage, being associated with both increased proinflammatory signaling and accumulation of neurotoxic metabolites. It is also hypothesized that ethanol-induced Zn deficiency may interfere with neurotransmission. Similar changes may take place in the fetus as a result of impaired placental zinc transfer, maternal zinc deficiency, or maternal Zn sequestration, resulting in fetal alcoholic syndrome. Therefore, alcoholic Zn deficiency not only mediates the adverse effects of ethanol exposure, but also provides an additional link between different alcohol-induced disorders. Generally, current findings suggest that assessment of Zn status could be used as a diagnostic marker of metabolic disturbances in alcohol abuse, whereas modulation of Zn metabolism may be a potential tool in the treatment of alcohol-associated disorders.

Zinc is a critical regulator of placental morphogenesis and maternal hemodynamics during pregnancy in mice

Zinc is an essential micronutrient in pregnancy and zinc deficiency impairs fetal growth. We used a mouse model of moderate zinc deficiency to investigate the physiological mechanisms by which zinc is important to placental morphogenesis and the maternal blood pressure changes during pregnancy. A 26% reduction in circulating zinc (P = 0.005) was exhibited in mice fed a moderately zinc-deficient diet. Zinc deficiency in pregnancy resulted in an 8% reduction in both near term fetal and placental weights (both P < 0.0001) indicative of disrupted placental development and function. Detailed morphological analysis confirmed changes to the placental labyrinth microstructure. Continuous monitoring of maternal mean arterial pressure (MAP) revealed a late gestation decrease in the zinc-deficient dams. Differential expression of a number of regulatory genes within maternal kidneys supported observations on MAP changes in gestation. Increased MAP late in gestation is required to maintain perfusion of multiple placentas within rodent pregnancies. Decreased MAP within the zinc-deficient dams implies reduced blood flow and nutrient delivery to the placenta. These findings show that adequate zinc status is required for correct placental morphogenesis and appropriate maternal blood pressure adaptations to pregnancy. We conclude that insufficient maternal zinc intake from before and during pregnancy is likely to impact in utero programming of offspring growth and development largely through effects to the placenta and maternal cardiovascular system.

Maternal Serum Iron and Zinc Levels and Gestational Diabetes

Gestational diabetes, a metabolic disturbance in pregnancy has many predisposing factors such as maternal age, history of gestational diabetes, familial history of diabetes, and obesity. There have been many studies performed all over the world to recognize more risk factors for gestational diabetes in order to better control it. Micronutrients such as iron and zinc status in the body are good examples in this regard. The studies have shown that despite the increased need for iron during pregnancy, if there is an iron overload in body, it may predispose the mother to gestational diabetes; but there has been no significant relationship observed between body zinc status and gestational diabetes occurrence. Thus, medical practitioners should consider checking the iron status of pregnant women before giving iron supplements to them.

The Relationship between Cord Blood and Maternal Serum Zinc Levels and Birth Weight

Background: Examining the relationship between cord blood and maternal serum zinc levels and birth weight.Methods: A total of 127 infant-mother pairs were assigned to study (n = 58; with birth weight < 2500 g) and control (n = 69; with birth weight ≥ 2500 g) groups. Serum samples were collected from eligible mothers and cord blood of their low birth weight (LBW) or normal birth weight (NBW) healthy newborns. The inclusion criterion for the infant-mother pairs was lack of any medical complications. Serum zinc level was measured by using Inductively Coupled Plasma Mass Spectrometer method and the results were expressed in μg/dl. The two groups were compared in terms of maternal and cord blood serum zinc levels. Then, we evaluated their association with birth weight of neonates in both groups through Student’s t-test and one-way analysis of variance using SPSS.Results: The study protocol was reviewed and approved by the ethics committee of the Urmia University of Medical Sciences (Ir.umsu.rec.1393.108 1393/04/24). Participants were provided with detailed information about the study and were assured that confidentiality would be maintained at all times. Written consent was obtained prior to data collection.The mean age of the pregnant women was 26.1±5.8 years (age range: 18-40 years). The mean birth weight of the neonates in the two groups was 3275.9±552 kg. Pregnant women with serum zinc levels of higher than 70 μg/dl gave birth to neonates with birth weight higher than 3.5, whereas mothers with serum zinc levels of less than 60 μg/dl gave birth to infants with birth weight less than 3 kg (P=0.034). Mean serum zinc level in the cord blood of LBW group was 79.16±19.86 μg/dl, which was significantly lower than that in the NBW group (95.14±17.56 μg/dl; P<0.021). Similarly, mean maternal serum zinc level was 63.98±19.33 μg/dl in mothers who gave birth to LBW neonates, while it was 86.13±20.10 μg/dl in mothers with NBW neonates, indicating that serum zinc level was significantly lower in mothers with LBW infants than in those with NBW infants (P=0.017).Conclusion: Maternal and cord blood zinc concentrations were shown to be associated with birth weight of the newborns

MRNA Levels of Placental Iron and Zinc Transporter Genes Are Upregulated in Gambian Women with Low Iron and Zinc Status

Background: The role of the placenta in regulating micronutrient transport in response to maternal status is poorly understood.Objective: We investigated the effect of prenatal nutritional supplementation on the regulation of placental iron and zinc transport.Methods: In a randomized trial in rural Gambia [ENID (Early Nutrition and Immune Development)], pregnant women were allocated to 1 of 4 nutritional intervention arms: 1) iron and folic acid (FeFol) tablets (FeFol group); 2) multiple micronutrient (MMN) tablets (MMN group); 3) protein energy (PE) as a lipid-based nutrient supplement (LNS; PE group); and 4) PE and MMN (PE+MMN group) as LNS. All arms included iron (60 mg/d) and folic acid (400 μg/d). The MMN and PE+MMN arms included 30 mg supplemental Zn/d. In a subgroup of ∼300 mother-infant pairs, we measured maternal iron status, mRNA levels of genes encoding for placental iron and zinc transport proteins, and cord blood iron levels.Results: Maternal plasma iron concentration in late pregnancy was 45% and 78% lower in the PE and PE+MMN groups compared to the FeFol and MMN groups, respectively (P < 0.001). The mRNA levels of the placental iron uptake protein transferrin receptor 1 were 30–49% higher in the PE and PE+MMN arms than in the FeFol arm (P < 0.031), and also higher in the PE+MMN arm (29%; P = 0.042) than in the MMN arm. Ferritin in infant cord blood was 18–22% lower in the LNS groups (P < 0.024). Zinc supplementation in the MMN arm was associated with higher maternal plasma zinc concentrations (10% increase; P < 0.001) than in other intervention arms. mRNA levels for intracellular zinc-uptake proteins, in this case zrt, irt-like protein (ZIP) 4 and ZIP8, were 96–205% lower in the PE+MMN arm than in the intervention arms without added zinc (P < 0.025). Furthermore, mRNA expression of ZIP1 was 85% lower in the PE+MMN group than in the PE group (P = 0.003).Conclusion: In conditions of low maternal iron and in the absence of supplemental zinc, the placenta upregulates the gene expression of iron and zinc uptake proteins, presumably in order to meet fetal demands in the face of low maternal supply. The ENID trial was registered at www.controlled-trials.com as ISRCTN49285450.

Effects of Maternal Zinc Glycine on Mortality, Zinc Concentration, and Antioxidant Status in a Developing Embryo and 1-Day-Old Chick.

This study was conducted to investigate the effects of maternal zinc glycine (Zn-Gly) supplementation as an alternative for zinc sulfate (ZnSO4) on mortality, zinc (Zn) concentration, and antioxidant status in a developing embryo and 1-day-old chick. Six hundred 39-week-old broiler breeders were randomly assigned to 6 treatments, each treatment including 5 replicates with 20 birds each. Six treatments received a basal diet (control, 24mg Zn/kg diet) or a basal diet supplemented with ZnSO4 (80mg Zn/kg) or Zn-Gly (20, 40, 60, or 80mg Zn/kg), respectively. The experiment lasted for 8weeks after a 4-week pre-experiment with a basal diet. At the last week, 100 eggs per replicate were randomly collected for incubation. Compared with the control treatment, Zn supplementation decreased (P<0.05) embryo mortalities of the late stage and the whole period, increased (P<0.05) liver Zn concentration in the embryo of d9, d19, and 1-day-old chick, and improved (P<0.05) antioxidant status in the embryo of d19 and 1-day-old chick. Compared with the ZnSO4 treatment, 80mg Zn/kg Zn-Gly treatment significantly decreased (P<0.05) the late stage embryo mortality and increased (P<0.05) liver Zn concentration in the embryo of d9, d19, and 1-day-old chick. The 80mg Zn/kg Zn-Gly treatment significantly increased (P<0.05) copper-zinc superoxide dismutase activity in d19 embryo and 1-day-old chick, total superoxide dismutase activity in 1-day-old chick, and copper-zinc superoxide dismutase messenger RNA (mRNA) abundance of d9 embryo and 1-day-old chick than that in ZnSO4 treatment. The liver metallothionein concentration of the developing embryo and 1-day-old chick and its mRNA abundance of d19 embryo were also significantly increased (P<0.05) in the 80mg Zn/kg Zn-Gly treatment in comparison with ZnSO4 treatment. In conclusion, maternal Zn supplementation decreased embryo mortalities of the late stage and the whole period by increasing liver Zn concentration and antioxidant status in d19 embryo and 1-day-old chick, and 80mg Zn/kg from Zn-Gly treatment was the optimum choice.

Impact of maternal and postnatal zinc dietary status on the prostate of pubescent and adult rats.

Zinc is important for cell physiology and alteration of its levels during development can modulate a series of biological events. The aim of this study was to investigate whether dietary zinc deficiency or supplementation during morphogenesis and early postnatal development could interfere in prostate maturation. Pregnant rats were exposed to a standard diet (NZ:35 mg Zn/kg chow), low-zinc diet (LZ:3 mg of Zn/kg chow) and zinc-supplemented diet (HZ:180 mg/Kg chow) from gestational day 10 (GD10) through postnatal day 21 (PND21). After weaning, male offspring were divided into three groups that were submitted to the same food conditions as their mothers until PND53. The animals were euthanized at PND53 and PND115. The ventral prostate was removed, weighed and its fragments were subjected to histological, western blot and zymography analysis. PND53: body and prostate weight were lower in LZ compared to NZ; the epithelial compartment was reduced while the stromal compartment was increased in LZ compared to NZ; there was an increase in the amount of collagen and reduction in AR and SIRT1 expression in LZ compared to NZ. PND115: body weight was lower in LZ compared to NZ and prostate weight was similar among the groups; peripheral physiological hyperplasia was observed, as well as an increased epithelial proliferation index and reduced PAR4 expression in LZ and HZ compared to NZ. Zinc deficiency during prostate morphogenesis and differentiation is potentially harmful to its morphology, however, by restoring the standard dietary environment, the gland responds to the new microenvironment independent of the previous dietary condition.

Association of Maternal Zinc Status and Fetal Outcome

Background: Maternal zinc is related to the growth and development of newborn babies. Low birth weight babies leads to higher infant mortality rate &amp; unfortunately the incidence of LBW is higher in Bangladesh.Objective: The present study has been undertaken to evaluate the zinc status in mothers with normal and low birth weight as well as to find-out the association between maternal zinc level and birth weight of babies in a selected hospital in Dhaka city.Methods: This case-control study on 20 non-pregnant and 40 pregnant women was done to find out the relationship between maternal zinc status and fetal outcome. This study was carried out in the department of Biochemistry, Dhaka Medical College, Dhaka, in collaboration with Bangladesh Atomic Energy Center, Dhaka from the period of July 2003 to June 2004.Result: The mean age (yrs), height (cms) &amp; parity (number) in Group-A found to be 23.7 ± 4.8, 154 ± 7 and 1.82 ± 0.85 respectively &amp; those in Group-B were 24.5 ± 4.3, 153 ± 9 and 1.86 ± 0.89 respectively without any significant difference between the groups. The mean plasma zinc concentrations in Control &amp; Cases were 90.10 ± 13.96 and 64.54 ± 16.22 ?g/dl respectively. The mean plasma zinc concentrations in Subgroup B-I &amp; B-II were 63.85 ± 12.49 and 65.18 ± 18.48 ?g/dl respectively.Conclusion: Maternal zinc status is not associated with fetal outcomes.J Shaheed Suhrawardy Med Coll, June 2014, Vol.6(1); 7-10

Adverse effects of parental zinc deficiency on metal homeostasis and embryonic development in a zebrafish model

The high prevalence of zinc deficiency is a global public health concern, and suboptimal maternal zinc consumption has been associated with adverse effects ranging from impaired glucose tolerance to low birthweights. The mechanisms that contribute to altered development and poor health in zinc deficient offspring are not completely understood. To address this gap, we utilized the Danio rerio model and investigated the impact of dietary zinc deficiency on adults and their developing progeny. Zinc deficient adult fish were significantly smaller in size, and had decreases in learning and fitness. We hypothesized that parental zinc deficiency would have an impact on their offspring's mineral homeostasis and embryonic development. Results from mineral analysis showed that parental zinc deficiency caused their progeny to be zinc deficient. Furthermore, parental dietary zinc deficiency had adverse consequences for their offspring including a significant increase in mortality and decreased physical activity. Zinc deficient embryos had altered expression of genes that regulate metal homeostasis including several zinc transporters (ZnT8, ZnT9) and the metal-regulatory transcription factor 1 (MTF-1). Zinc deficiency was also associated with decreased expression of genes related to diabetes and pancreatic development in the embryo (Insa, Pax4, Pdx1). Decreased expression of DNA methyltransferases (Dnmt4, Dnmt6) was also found in zinc deficient offspring, which suggests that zinc deficiency in parents may cause altered epigenetic profiles for their progeny. These data should inform future studies regarding zinc deficiency and pregnancy and suggest that supplementation of zinc deficient mothers prior to pregnancy may be beneficial.

Maternal dietary zinc supplementation enhances the epigenetic-activated antioxidant ability of chick embryos from maternal normal and high temperatures.

The role of maternal dietary zinc supplementation in protecting the embryos from maternal hyperthermia-induced negative effects via epigenetic mechanisms was examined using an avian model (Gallus gallus). Broiler breeder hens were exposed to two maternal temperatures (21°C and 32°C) × three maternal dietary zinc treatments (zinc-unsupplemented control diet, the control diet + 110 mg zinc/kg inorganic or organic zinc) for 8 weeks. Maternal hyperthermia increased the embryonic mortality and induced oxidative damage evidenced by the elevated mRNA expressions of heat shock protein genes. Maternal dietary zinc deficiency damaged the embryonic development associated with the global DNA hypomethylation and histone 3 lysine 9 hyperacetylation in the embryonic liver. Supplementation of zinc in maternal diets effectively eliminated the embryonic mortality induced by maternal hyperthermia and enhanced antioxidant ability with the increased mRNA and protein expressions of metallothionein IV in the embryonic liver. The increased metallothionein IV mRNA expression was due to the reduced DNA methylation and increased histone 3 lysine 9 acetylation of the metallothionein IV promoter regardless of zinc source. These data demonstrate that maternal dietary zinc addition as an epigenetic modifier could protect the offspring embryonic development against maternal heat stress via enhancing the epigenetic-activated antioxidant ability.

Combined Effects of Gestational Phthalate Exposure and Zinc Deficiency on Steroid Metabolism and Growth.

Disruption of steroid hormone signaling has been implicated independently in the developmental abnormalities resulting from maternal phthalate plasticizer exposure and developmental zinc deficiency. This study investigated if secondary zinc deficiency may result from dietary exposure to a low level of di-2-ethylhexyl phthalate (DEHP) through gestation and if this could be associated with altered steroid metabolism. The interaction between marginal zinc nutrition and DEHP exposure to affect pregnancy outcome, zinc status, and steroid metabolism was also assessed. For this purpose, rats were fed a diet containing an adequate (25 mg/kg) or marginal (10 mg/kg) level of zinc without or with DEHP (300 mg/kg) from gestation day (GD) 0 until GD 19. Steroid profiles were measured in dam liver, plasma, adrenal glands, and in fetal liver by UPLC/MS-MS. In dams fed the adequate zinc diet, DEHP exposure decreased maternal weight gain and led to hepatic acute-phase response and zinc accumulation. The latter could compromise zinc availability to the fetus. DEHP and marginal zinc deficiency caused several adverse effects on the maternal and fetal steroid profiles. Interactions between DEHP exposure and marginal zinc deficient nutrition affected 17OH pregnenolone and corticosterone, while pregnenolone levels were specifically affected by DEHP exposure. Maternal marginal zinc deficiency specifically affected maternal progesterone and aldosterone, and presented evidence of increased androgen aromatization activity in maternal and fetal tissues. Results stress the potential major impact of mild DEHP exposure on maternal/fetal steroid metabolism that can be potentiated by nutritional and chronic disease states leading to zinc deficiency.

Zinc deficiency affects the STAT1/3 signaling pathways in part through redox-mediated mechanisms

Zinc deficiency affects the development of the central nervous system (CNS) through mechanisms only partially understood. We previously showed that zinc deficiency causes CNS oxidative stress, damaging microtubules and impairing protein nuclear shuttling. STAT1 and STAT3 transcription factors, which require nuclear import for their functions, play major roles in CNS development. Thus, we investigated whether zinc deficiency disrupts STAT1 and STAT3 signaling pathways in the developing fetal CNS, characterizing the involvement of oxidative stress and the cytoskeleton in the adverse effects. Maternal (gestation day 0–19) marginal zinc deficiency (MZD) reduced STAT1 and STAT3 tyrosine phosphorylation and their nuclear translocation in the embryonic day 19 (E19) rat brain. Similar effects were observed in zinc depleted IMR-32 neuroblastoma cells, with an associated decrease in STAT1- and STAT3-dependent gene transactivation. Zinc deficiency caused oxidative stress (increased 4-hydroxynonenal-protein adducts) in E19 brain and IMR-32 cells, which was prevented in cells by supplementation with 0.5mM α-lipoic acid (LA). In zinc depleted IMR-32 cells, the low tyrosine phosphorylation of STAT1, but not that of STAT3, recovered upon incubation with LA. STAT1 and STAT3 nuclear transports were also restored by LA. Accordingly, chemical disruption of the cytoskeleton partially reduced STAT1 and STAT3 nuclear levels. In summary, the redox-dependent tyrosine phosphorylation, and oxidant-mediated disruption of the cytoskeleton are involved in the deleterious effects of zinc deficit on STAT1 and STAT3 activation and nuclear translocation. Therefore, disruption of the STAT1 and STAT3 signaling pathways may in part explain the deleterious effects of maternal MZD on fetal brain development.

Associations of Maternal Serum Zonulin and Elements Concentrations with Neonatal Birth Weight: A Case-Control Study

Introduction: Intake of micronutrients and zonulin levels (as a marker for intestinal permeability) during pregnancy can be effective on birth weight of infants. However, no studies have investigated the relationship between the infants birth weight and maternal zonulin level. Aim: This study aimed to compare the zonulin levels and maternal trace elements in infants with low birth weight (LBW) and Normal Birth Weight (NBW) and its relationship with weight, length and head circumference of infants. Materials and Methods: In this study, 368 infants were divided into two groups: case (n=82) with birth weight of = 2500 gm. Maternal zonulin, zinc, calcium, copper and iron levels were evaluated. Weight, length and head circumference of infants were measured. The maternal serum level zonulin and micronutrients between the two groups were assessed using Student t-test or Chi-squared test and the relationship between variables using Spearman's rank correlation. Results: A significant difference was seen in the maternal zonulin and zinc serum levels between the LBW and the NBW infants (<0.001). No significant difference was observed in the calcium, copper, and iron levels between the two groups. A significant positive relationship was seen between maternal serum zonulin and zinc concentration with the birth weight of the LBW infants (respectively r=0.45 and r=0.41) (p<0.05). No relationship was seen between maternal serum zonulin and zinc concentration with the length and head circumference of the infants. Conclusion: The results showed that the maternal serum Zn level is associated with the infants birth weight. In addition, intestinal permeability, as a new factor could affect the birth weight and birth rate of the LBW infants. Further studies in this area are recommended.

Correlation of Pregnancy Associated Plasma Protein A and Zinc with Calculated Risk Ratio of Dual Test.

First trimester screening by dual test is the most preferred method of antenatal screening. The detection rate of foetal aneuploidy using dual test is 95%. This test uses maternal serum free β human Chorionic Gonadotropin (free β hCG) and Pregnancy Associated Plasma Protein A (PAPP-A) along with maternal demographic and foetal sonographic indices to calculate risk for foetal aneuploidy. PAPP-A is a zinc binding metalloproteinase which is also responsible for placental development and foetal growth. So, zinc might also have some role in first trimester screening. No studies are available substantiating the role of zinc in first trimester screening. To measure and correlate maternal serum zinc with PAPP-A and calculated risk ratio of first trimester screening. PAPP-A and zinc were measured from the serum of 84 pregnant women aged 20-40 years in 11th-13th weeks+6 days of gestation who underwent dual test during their antenatal check-up. Risk calculation was done using Screening Software for Downs Windows Lab (SSDWL). Maternal serum PAPP-A showed a significant positive correlation with maternal serum zinc (p-value <0.001). Maternal serum PAPP-A and zinc both showed a significant positive correlation with calculated risk ratio (p-value<0.01). As PAPP-A is a zinc binding metalloproteinase, zinc showed significant pattern of correlation with aneuploidy risk as shown by PAPP-A. So there could be a possible role for serum zinc in first trimester of screening.

Identification of Genetic Diseases Using Breast Milk Cell Analysis: The Case of Transient Neonatal Zinc Deficiency (TNZD)

Infants exclusively breastfed with zinc-deficient milk, develop transient neonatal zinc deficiency (TNZD) due to inactivating mutations in the maternal zinc transporter SLC30A2/ZnT2. In the current study, DNA sequencing of SLC30A2/ ZnT2 in a mother exclusively breastfeeding her infant which presented with TNZD symptoms, identified a single nucleotide missense mutation c.839G>T. This mutation was initially predicted to result in a single amino acid substitution p.(Gly280Val). However, c.838G was also predicted to be located close to a splice site. Hence, using sequencing of mRNA isolated from the mother’s breast milk cells, we discovered that the c.839G>T mutation creates an alternative 3’-splice sites, introducing a 27 bp exon skipping. This mutant protein lacking 9 amino acids (Δ9AA) failed to dimerize with the wild type (WT) ZnT2 protein and displayed enhanced degradation. Furthermore, the zinc transport ability of this mutant protein was completely lost as shown by intracellular zinc accumulation using the zinc fluorescent probes Zinquin and Fluozin 3 AM. These findings reveal that the Δ9AA-ZnT2 variant did not exert a dominant negative effect over the WT ZnT2 protein. Hence, we provide direct evidence that a haploinsufficiency state occurs in women with heterozygous SLC30A2/ZnT2 mutations. Importantly, we herein developed a novel genetic test of expressed genes using maternal breast milk cells, which is well suited for the early diagnosis and prevention of TNZD and possibly other micronutrient deficiencies.

Maternal zinc deficiency and congenital anomalies in newborns.

Zinc deficiency in pregnant women is common, especially in the third trimester of pregnancy. The available data, however, on the association between zinc deficiency and congenital malformations in the Iranian population are insufficient. The aim of this study was therefore to determine whether maternal serum zinc deficiency is associated with major congenital malformations in newborns. This descriptive, case-control study involved mothers of 80 neonates with congenital anomalies (study group) admitted to the Mofid Children's Hospital, Tehran, Iran. During the same period (2014 and 2015), serum zinc was measured in 80 mothers who had delivered normal newborns without congenital malformations (control group). Mothers with serum zinc deficiency had a more than sevenfold risk of malformations in the fetus compared with mothers with normal serum zinc (OR, 7.013; 95%CI: 2.716-18.110). Newborns with malformation weighing ≤2500 g were associated with lower maternal serum zinc compared with the control group (P = 0.006). There is an association between congenital malformation in newborns and maternal zinc deficiency.

Effect of maternal zinc supplementation on the cardiometabolic profile of Peruvian children: results from a randomized clinical trial.

Zinc is an essential micronutrient for the development of the fetal renal, cardiovascular and metabolic systems; however, there is limited evidence of its effects on the postnatal cardiometabolic function. In this study, we evaluated the effect of maternal zinc supplementation during pregnancy on the cardiometabolic profile of the offspring in childhood. A total of 242 pregnant women were randomly assigned to receive a daily supplement containing iron+folic acid with or without zinc. A follow-up study was conducted when children of participating mothers were 4.5 years of age to evaluate their cardiometabolic profile, including anthropometric measures of body size and composition, blood pressure, lipid profile and insulin resistance. No difference in measures of child cardiometabolic risk depending on whether mothers received supplemental zinc during pregnancy. Our results do not support the hypothesis that maternal zinc supplementation reduces the risk of offspring cardiometabolic disease.

Association between Maternal Zinc Status, Dietary Zinc Intake and Pregnancy Complications: A Systematic Review.

Adequate zinc stores in the body are extremely important during periods of accelerated growth. However, zinc deficiency is common in developing countries and low maternal circulating zinc concentrations have previously been associated with pregnancy complications. We reviewed current literature assessing circulating zinc and dietary zinc intake during pregnancy and the associations with preeclampsia (PE); spontaneous preterm birth (sPTB); low birthweight (LBW); and gestational diabetes (GDM). Searches of MEDLINE; CINAHL and Scopus databases identified 639 articles and 64 studies were reviewed. In 10 out of 16 studies a difference was reported with respect to circulating zinc between women who gave birth to a LBW infant (≤2500 g) and those who gave birth to an infant of adequate weight (>2500 g), particularly in populations where inadequate zinc intake is prevalent. In 16 of our 33 studies an association was found between hypertensive disorders of pregnancy and circulating zinc; particularly in women with severe PE (blood pressure ≥160/110 mmHg). No association between maternal zinc status and sPTB or GDM was seen; however; direct comparisons between the studies was difficult. Furthermore; only a small number of studies were based on women from populations where there is a high risk of zinc deficiency. Therefore; the link between maternal zinc status and pregnancy success in these populations cannot be established. Future studies should focus on those vulnerable to zinc deficiency and include dietary zinc intake as a measure of zinc status.

Early Life Predictors of Socio-Emotional Development in a Sample of Egyptian Infants.

IntroductionEmotional problems are amongst the most critical concerns to be intentionally handled to enhance the wellbeing and development of children.ObjectiveTo determine the predictors of socio-emotional development of Egyptian infants related to infant feeding practices, aspects of infant and maternal health and socioeconomic status.Subjects and MethodsA cross-sectional comparative study included 322 breast fed, 240 bottle fed and 93 mixed fed infants, from 6–24 months of age, who were enrolled in the Well–Baby Clinic of the National Research Centre and from pediatric outpatient facilities in urban Cairo. Assessment of socio-emotional development was performed using Bayley Scales of Infant and Toddler Development (Bayley III). Detailed maternal and infant history was recorded. Levels of serum zinc, copper, iron, vitamin B12 and complete blood count (CBC) were assessed in a subsample of 193 infants.ResultsThe risk of having below average socio-emotional composite score was nearly two and half times among formula-fed infants than among breast-fed infants. By binary logistical regression analysis, predictors of below average socio-emotional score were a lower serum zinc value, being formula fed during the first half-year and introduction of complementary food before the age of six months (p< 0.05).ConclusionExclusive breastfeeding and to a lesser extent mixed feeding during the first half year is correlated with above average socio-emotional development. Maternal education and zinc status were also determinants of better infant mental health. Our endeavors ought to be directed towards integrated interventions addressing multiple risks to children’s development.