Iron deficiency during pregnancy affects postnatal blood pressure in the rat

Gambling, Lorraine; Dunford, Susan; Wallace, Donna; Zuur, Grietje; Solanky, Nita; Srai, Surjit Kaila; McArdle,

doi:10.1111/j.1469-7793.2003.00603.x

Cited by 70 publications

(47 citation statements)

References 36 publications

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“…The early period (days 0-7) corresponds to the embryonic phase of development in the rat and in fact embryos only implant at around day 4.5. 7 The mid-gestation period (days [8][9][10][11][12][13][14] largely corresponds to the period of organogenesis, while late gestation (days [15][16][17][18][19][20][21][22] is the period of most rapid growth and differentiation of key structures. By feeding at these targeted periods, it is possible to identify when nutritional programming occurs and this can provide important indicators of potential mechanisms.…”

Section: Animalsmentioning

confidence: 99%

“…A large number of studies in rats, mice, guinea pigs and sheep have clearly shown that exposure to relatively short periods of undernutrition or endocrine disturbance in fetal life can programme raised blood pressure, glucose intolerance and insulin resistance. [7][8][9] The range of nutritional exposures capable of eliciting programmed responses in the developing offspring is broad, including micronutrient deficiency, [10][11][12] excess of saturated fat 13 and restriction of food intake (global nutrient restriction). 14,15 In the present paper, we report findings from a model of low protein feeding in rat pregnancy.…”

Section: Introductionmentioning

confidence: 99%

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Exposure to undernutrition in fetal life determines fat distribution, locomotor activity and food intake in ageing rats

2006

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Objective: To assess the long-term impact of undernutrition during specific periods of fetal life, upon central adiposity, control of feeding behaviour and locomotor activity. Design: Pregnant rats were fed a control or low-protein (LP) diet, targeted to early (LPE), mid (LPM) or late (LPL) pregnancy or throughout gestation (LPA). The offspring were studied at 9 and 18 months of age. Measurements: Adiposity was assessed by measuring weight of abdominal fat depots relative to body weight. Locomotor activity was assessed using an infrared sensor array system in both light and dark conditions. Hypothalamic expression of mRNA for galanin and the galanin 2 receptor (Gal2R) was determined using real-time PCR. Results: At 9 months, male rats exposed to LP in utero had less fat in the gonadal depot, but were of similar body weight to controls. By 18 months, the males of groups LPA and LPM had more abdominal and less subcutaneous fat. Females deposited more fat centrally than males between 9 and 18 months of age, and this was more marked in groups LPA and LPL. Food intake was greater in LPM males. Among females hypophagia was noted in groups LPA and LPL. Expression of galanin and Gal2R were unaffected by maternal diet. Total locomotor activity was reduced in LPE males and all LP females in the light but not in the dark. Conclusion: Locomotor activity and feeding behaviour in aged rats are subject to prenatal programming influences. Fetal undernutrition does not programme obesity in rats without postnatal dietary challenge.

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Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exposure to undernutrition in fetal life determines fat distribution, locomotor activity and food intake in ageing rats

2006

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“…In female offspring, the prenatal treatment induces a lower systolic pressure before puberty, but afterwards, the results mirror those of the male offspring (23) . The different effects on females have not been followed up, but more recent evidence suggests that there are important differences in the prenatal programming consequences for male and female offspring in response to a variety of nutritional stresses (24) .…”

Section: Consequences Of Deficiencymentioning

confidence: 74%

“…The effect of iron deficiency on gene expression As discussed earlier, iron deficiency during pregnancy results in symptoms of metabolic syndrome in rats, with increased blood pressure, obesity and changed lipid metabolism in the offspring (23) . These results mimic those seen in rodents fed a low-protein diet (33) , and the similarities led us to the hypothesis that there may be common pathways or gene changes affected by disparate nutritional stresses, which we called the Table 1.…”

Section: Proceedings Of the Nutrition Societymentioning

confidence: 94%

Iron deficiency during pregnancy: the consequences for placental function and fetal outcome

2013

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This review examines the importance of the placenta in iron metabolism during development and the effect of iron deficiency on maternal and fetal physiology. Iron is an essential micronutrient, required for a wide variety of biological processes. During pregnancy, the mother has to deplete her iron stores in order to provide the baby with adequate amounts. Transplacental iron transfer involves binding transferrin (Tf)-bound iron to the Tf receptor, uptake into an endosome, acidification, release of iron through divalent metal transporter 1, efflux across the basolateral membrane through ferroportin and oxidation of Fe(II) by zyklopen. An additional haem transport system has been hypothesised, which may explain why certain gene knockouts are not lethal for the developing fetus. Iron deficiency is a common phenomenon during pregnancy, and the placenta adapts by up-regulating its transfer systems, maintaining iron at the expense of the mother. Despite these adaptations, deficiency cannot be completely prevented, and the offspring suffers both short-and long-term consequences. Some of these, at least, may arise from decreased expression of genes involved in the cell cycle and altered expression of transcription factors, such as c-myc, which in turn can produce, for example, kidneys with reduced numbers of nephrons. The mechanism whereby these changes are induced is not certain, but may simply be as a result of the reduced availability of iron resulting in decreased enzyme activity. Since these changes are so significant, and because some of the changes are irreversible, we believe that iron prophylaxis should be considered in all pregnancies.

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“…Pregnant rats fed a low-protein diet give birth to offspring that develop hypertension, which persists into adult life (14) . Indeed, some or all the components of the metabolic syndrome can be produced by a variety of maternal exposures, including global nutrient restriction (15) , placental insufficiency (16) and a low-Fe diet (17) as well as a low-protein diet. The animal data have allowed for increasingly sophisticated exploration of potential mechanisms and have greatly enhanced the DOHaD field.…”

Section: Developmental Origins Of Health and Disease: Maternal Supplementioning

confidence: 99%

Exploiting dietary supplementation trials to assess the impact of the prenatal environment on CVD risk

Hawkesworth

2008

Proc. Nutr. Soc.

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Animal studies have demonstrated that altering the maternal diet during pregnancy affects offspring disease risk. Data from human subjects on the early-life determinants of disease have been derived primarily from birth-weight associations; studies of the impact of the maternal diet are scarce and inconsistent. Investigating CVD risk factors in the offspring of women who have participated in maternal supplementation trials provides a useful resource in this research field, by virtue of employing an experimental design (as compared with observational studies). To date, follow-up studies have been published only for a small number of trials; these trials include the impact of maternal protein-energy, multiple-micronutrient and Ca supplementation on offspring disease risk. In Nepal maternal micronutrient supplementation has been shown to be associated with lower offspring systolic blood pressure at 2 years of age. Data from Guatemala on a pre-and postnatal protein-energy community intervention have suggested longterm improvements in fasting glucose and body composition but not in blood pressure. In The Gambia no association has been found between prenatal protein-energy supplementation and markers of CVD risk including body composition, blood pressure and fasting glucose and insulin in childhood and adolescence. Little evidence of an effect of maternal Ca supplementation on offspring blood pressure has been demonstrated in four trials, although the risk of high systolic blood pressure was found to be reduced in one trial. The present paper reviews the current evidence relating maternal nutritional supplementation during pregnancy to offspring CVD risk and explores the potential explanations for the lack of association.Developmental origins of health and disease: Maternal supplementation trials: CVD risk

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Iron deficiency during pregnancy affects postnatal blood pressure in the rat

Cited by 70 publications

References 36 publications

Exposure to undernutrition in fetal life determines fat distribution, locomotor activity and food intake in ageing rats

Exposure to undernutrition in fetal life determines fat distribution, locomotor activity and food intake in ageing rats

Iron deficiency during pregnancy: the consequences for placental function and fetal outcome

Exploiting dietary supplementation trials to assess the impact of the prenatal environment on CVD risk

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