Fetal and postnatal zinc restriction: sex differences in the renal renin-angiotensin system of newborn and adult Wistar rats.

This study aimed to evaluate renal morphology and the renal renin-angiotensin system in 6- and 81-day-old male and female offspring exposed to zinc deficiency during fetal life, lactation and/or postnatal growth. Female Wistar rats were fed low- or control zinc diets from pregnancy to offspring weaning. Afterwards, offspring were fed a low- or a control zinc diet until 81 days of life.

Fetal and postnatal zinc restriction: Sex differences in metabolic alterations in adult rats.

Objective: Intrauterine and postnatal micronutrient malnutrition may program metabolic diseases in adulthood. We examined whether moderate zinc restriction in male and female rats throughout fetal life, lactation, or postweaning growth induces alterations in liver, adipose tissue, and intermediate metabolism.

Methods: Female Wistar rats were fed low-zinc or control zinc diets from pregnancy to offspring weaning.

Developmental programming of vascular dysfunction by prenatal and postnatal zinc deficiency in male and female rats.

Micronutrient malnutrition during intrauterine and postnatal growth may program cardiovascular diseases in adulthood. We examined whether moderate zinc restriction in male and female rats throughout fetal life, lactation and/or postweaning growth induces alterations that can predispose to the onset of vascular dysfunction in adulthood. Female Wistar rats were fed low- or control zinc diets from pregnancy to offspring weaning.

Cardiac changes in apoptosis, inflammation, oxidative stress, and nitric oxide system induced by prenatal and postnatal zinc deficiency in male and female rats.

Purpose: Zinc restriction during fetal and postnatal development could program cardiovascular diseases in adulthood. The aim of this study was to determine the effects of zinc restriction during fetal life, lactation, and/or post-weaning growth on cardiac inflammation, apoptosis, oxidative stress, and nitric oxide system of male and female adult rats.

Methods: Wistar rats were fed a low- or a control zinc diet during pregnancy and up to weaning.

Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences.

Background: A substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may "program" susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases.

Materials And Methods: This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults.

Morphological and functional effects on cardiac tissue induced by moderate zinc deficiency during prenatal and postnatal life in male and female rats.

The aim of this study was to evaluate whether moderate zinc restriction in rats throughout fetal life, lactation, and/or postweaning growth results in early changes in cardiac morphology predisposing the onset of cardiac dysfunction in adult life as well as sex-related differences in the adaptation to this nutritional injury. Female Wistar rats received low or control zinc diets from the beginning of pregnancy up to offspring weaning. After being weaned, offspring were fed either a low or control zinc diet until 81 days.

Mild zinc deficiency in male and female rats: early postnatal alterations in renal nitric oxide system and morphology.

Objective: Fetal and postnatal zinc deficiencies induce an increase in arterial blood pressure and impair renal function in male adult rats. We therefore hypothesized that these renal alterations are present in early stages of life and that there are sexual differences in the adaptations to this nutritional injury. The aim was to study the effects of moderate zinc deficiency during fetal life and lactation on renal morphology, oxidative stress, apoptosis, and the nitric oxide system in male and female rats at 21 d of life.

Zinc restriction during different periods of life: influence in renal and cardiovascular diseases.

Micronutrient undernutrition during critical periods of growth has become an important health issue in developing and developed countries, particularly among pregnant women and children having an imbalanced diet. Zinc is a widely studied microelement in infant feeding because it is a component of several enzymes involved in intermediary metabolism ranging from growth to cell differentiation and metabolism of proteins, carbohydrates, and lipids. Human and experimental studies have reported an association between zinc deficiency and the etiopathogenesis of cardiovascular and renal diseases like hypertension, atherosclerosis, congestive heart failure, coronary heart disease, and diabetes.

Moderate zinc restriction during fetal and postnatal growth of rats: effects on adult arterial blood pressure and kidney.

Intrauterine and postnatal zinc restriction may result in an adverse environment for the development of cardiovascular and renal systems. This study evaluated the effects of moderate zinc deficiency during fetal life, lactation, and/or postweaning growth on systolic blood pressure, renal function, and morphology in adult life. Female Wistar rats received low (8 ppm) or control (30 ppm) zinc diets from the beginning of pregnancy up to weaning.

Zinc deficiency during growth: influence on renal function and morphology.

This study was designed to investigate the effects of moderate zinc deficiency during growth on renal morphology and function in adult life. Weaned male Wistar rats were divided into two groups and fed either a moderately zinc-deficient diet (zinc: 8 mg/kg, n=12) or a control diet (zinc: 30 mg/kg, n=12) for 60 days. We evaluated: renal parameters, NADPH-diaphorase and nitric oxide synthase activity in kidney, renal morphology and apoptotic cells in renal cortex.