The effect of regular maternal exercise on erythropoietin in cord blood and amniotic fluid

Clapp, James F.; Little, Kathleen D.; Appleby-Wineberg, S.; Widness, John A.

doi:10.1016/0002-9378(95)90476-x

Cited by 55 publications

(28 citation statements)

References 13 publications

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“…Intestinal cells are exposed to intraluminal Epo during fetal life because it is present in amniotic fluid (5,6), which is continually swallowed by the fetus. Intraluminal exposure to Epo continues postnatally as it is present in colostrum and breast milk.…”

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confidence: 99%

Origin and Fate of Erythropoietin in Human Milk

et al. 2000

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Erythropoietin (Epo) is a normal constituent of human milk, but the origin and fate of this cytokine in milk are not known. Regarding its origin, we hypothesized that cells of the mammary gland secrete Epo into milk actively and, therefore, that concentrations in milk do not correlate with concentrations in serum. Regarding its fate, we hypothesized that Epo concentrations in milk change with time postpartum and that Epo in milk is protected from digestion in the neonatal gastrointestinal tract. To address these issues, we measured Epo concentrations in 103 milk samples (ELISA), 55 of which were paired with serum. Mammary duct epithelial cells were evaluated as a source of Epo by breast tissue immunohistochemistry and by cell culture. Circulating and milk Epo were compared by Western analysis to detect size differences, possibly reflecting differences in processing. Epo stability in simulated conditions of digestion was evaluated. We observed that milk Epo concentrations increase as a function of duration of breast-feeding and have a negative correlation with serum Epo or milk protein concentration. Mammary duct epithelial cells from breast biopsies of lactating women had marked immunoreactivity to Epo, but such activity was minimal to absent in nonlactating breast tissue. Further evidence that mammary duct epithelia produce Epo was obtained by observing Epo mRNA and protein expression in cultured human mammary epithelial cells. The molecular size of Epo in milk and serum is identical. Recombinant Epo added to human milk or commercial infant formulas was relatively stable in conditions that simulate gastric and small intestinal conditions of newborn infants; however, recombinant Epo added to D 5 W was not protected from digestion. We conclude that Epo concentrations in milk increase as a function of the duration of breast feeding, that Epo is actively secreted into human milk by mammary duct epithelia, and that the Epo within milk is largely protected from digestion. Abbreviations Epo, erythropoietin Epo-R, erythropoietin receptors GI, gastrointestinal HMEC, human mammary epithelial cells rEpo, recombinant erythropoietin Significant Epo concentrations have been measured in human milk (1), but the origin and fate of Epo in milk are not known. Specifically, it is not known whether Epo is secreted actively or passively into milk, whether any Epo-producing cells exist in breast tissue, whether maternal serum Epo concentrations correlate with milk Epo concentrations, or whether milk Epo is processed differently from circulating Epo, resulting in a difference in glycosylation. In addition, it is not known whether Epo concentrates in a particular partition (fore, mid, or hind milk) or phase (aqueous versus lipid) of milk. No information is available regarding the stability of rEpo added to commercially available infant formulas or whether routine storage conditions (freeze/thaw) or pasteurization procedures (heating) degrade Epo.A physiologic role for enteral Epo is likely, as Epo-R are present on mucosal cells of the ...

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Origin and Fate of Erythropoietin in Human Milk

et al. 2000

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“…Some clinical reports suggested that EPO levels in both cord blood and amniotic fluid at birth are helpful in determining the timing of fetal hypoxia [14,15]. However, detailed data on the rates of appearance and turnover of amniotic fluid EPO compared to those of fetal serum EPO are not available.…”

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Effect of Hypoxia on Amniotic Fluid Erythropoietin Levels in Fetal Rats

Kakuya

Shirai²,

Takase³

et al. 1997

Neonatology

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Erythropoietin (EPO) levels in amniotic fluid and serum were measured in hypoxic (fraction of inspired oxygen, FiO₂, 0.09) and posthypoxic (following a 24-hour period of hypoxia, FiO₂ 0.09) fetal rats on day 21 of gestation. Each of the study groups comprised 12–20 fetuses. Each of the control groups consisted of 21 or 22 fetuses. Fetal serum EPO levels at 3, 6, 9, 12, and 24 h of hypoxia were significantly higher than the control level. Amniotic fluid EPO levels at 9, 12, and 24 h of hypoxia were also significantly increased compared to the control level. Fetal serum EPO levels returned to baseline during the 12- to 48-hour period after hypoxia. During the 0- to 48-hour posthypoxic period, amniotic fluid EPO levels were significantly higher than the control level. These data demonstrate that rates of appearance and turnover of amniotic fluid EPO are different from those of fetal serum EPO.

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“…The functional Epo receptors are also in the fetal and postnatal small bowel and their ligands are available for binding [8,9]. During fetal life, enterocytes are exposed to Epo because it exists in swallowed amniotic fluid [10,11]; in breast-fed infants, exposure to enteral Epo continues through the intake of mother's milk [12][13][14][15]. It is known that breast feeding and rEpo treatment decrease the incidence of NEC in premature infants [16,17], suggesting that Epo plays a role in the growth and development of the gastrointestinal tract.…”

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confidence: 99%

Erythropoietin Protects against Necrotizing Enterocolitis of Newborn Rats by the Inhibiting Nitric Oxide Formation

et al. 2003

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Background: Necrotizing enterocolitis (NEC) is an important neonatal disease with a high mortality rate; erythropoietin (Epo) is a hematopoietic growth factor. Functional Epo receptors are in the fetal and postnatal small bowel and their ligands are available for binding. Excessive nitric oxide (NO) production by an isoform of NO synthase inducible by inflammatory stimuli leads to changes in vascular permeability and tissue injury. The aim of this study was to investigate NO formation in an experimental model of NEC and the possible role of NO in the protection Epo provides against NEC. Methods: Twenty-four Wistar albino rat pups were divided into three groups: group 1 = control; group 2 = hypoxia-reoxygenation and saline; group 3 = hypoxia-reoxygenation and recombinant human EPO (rhEpo) pretreatment. rhEpo was given 750 U/kg/week by intraperitoneal injection 3 times a week for 2 weeks. On the 15th day, hypoxia was induced by placing the pups in a 100% CO₂ chamber for 5 min. After the hypoxia period the pups were reoxygenated for 10 min with 100% O₂ and returned to their mothers. All pups were killed 4 h after the hypoxia-reoxygenation period was over. The abdomen was opened and representative samples of injured areas were taken for histopathologic examination. Then nitrite levels were determined in the intestine by Griess Reagent. Results: On histopathological examination, injury scores in group-2 animals were found to be significantly higher than in group-3 animals (p = 0.001). Significantly increased intestinal nitrite levels were found in group-2 rats compared to the rats of groups 1 and 3 (p = 0.001 and p = 0.001, respectively). There was a positive correlation between the histological findings and the intestinal nitrite levels in group-2 and -3 animals (r = 0.94, p = 0.001; r = 0.99, p = 0.001, respectively). Conclusion: The present study demonstrates that the Epo-pretreated group had decreased levels of NO and limited mucosal necrosis in intestinal tissue samples. We believe that these results deserve further experimental studies in order to elucidate the possible effector mechanisms involved in the inhibitory relationship between Epo, NO and NEC.

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The effect of regular maternal exercise on erythropoietin in cord blood and amniotic fluid

Cited by 55 publications

References 13 publications

Origin and Fate of Erythropoietin in Human Milk

Origin and Fate of Erythropoietin in Human Milk

Effect of Hypoxia on Amniotic Fluid Erythropoietin Levels in Fetal Rats

Erythropoietin Protects against Necrotizing Enterocolitis of Newborn Rats by the Inhibiting Nitric Oxide Formation

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