ImpactofZincDeficiencyDuringPrenataland/or PostnatalLifeonCardiovascularandMetabolic Diseases:ExperimentalandClinicalEvidence

Abstract

This review summarizes the latest findings, from animal models and clinical studies, regarding the cardiovascular and metabolic consequences in adult life of zinc deficiency (ZD) during prenatal and early postnatal life. The effect of zinc supplementation (ZS) and new insights about sex differencesinthephenotypeandseverityofcardiovascularandmetabolicalterationsarealsodiscussed.Zinchasantioxidant,anti-inflammatory,and antiapoptoticpropertiesandregulatestheactivityofenzymesinvolvedinregulationofthemetabolic,cardiovascular,andrenalsystems.Maternal ZDisassociatedwithintrauterinegrowthrestrictionandlowbirthweight(LBW).Breast-fedpreterminfantsareatriskofZDduetolowerzincuptake duringfetallifeandreducedgutabsorptioncapacity.ZSismostlikelytoincreasegrowthinpreterminfantsandsurvivalinLBWinfantsincountries where ZD is prevalent. Studies performed in rats revealed that moderate ZD during prenatal and/or early postnatal growth is a risk factor for the development of hypertension, cardiovascular and renal alterations, obesity, and diabetes in adult life. An adequate zinc diet during postweaning life does not always prevent the cardiovascular and metabolic alterations induced by zinc restriction during fetal and lactation periods. Male rats are more susceptible to this injury than females, and some of the mechanisms involved include: 1) alterations in organogenesis, 2) activation of oxidative, apoptotic, and inflammatory processes, 3) dysfunction of nitric oxide and renin-angiotensin-aldosterone systems, 4) changes in glucose and lipid metabolism, and 5) adipose tissue dysfunction. Safeguarding body zinc requirements during pregnancy, lactation, and growth periods couldbecomeanewtargetinthepreventionandtreatmentofcardiovascularandmetabolicdisorders.Furtherresearchisneededtoelucidatethe efficacyofZSduringearlystagesofgrowthtopreventthedevelopmentofthesediseaseslaterinlife.