Transcriptional regulation of copper metabolism genes in the liver of fetal and neonatal control and iron-deficient rats

Lenartowicz, Małgorzata; Kennedy, Christine; Hayes, Helen; McArdle, Harry J

doi:10.1007/s10534-014-9802-z

Cited by 19 publications

(14 citation statements)

References 69 publications

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“…Evidence for altered trophoblastic invasion and vessel remodeling have been reported in a rat model of HFD induced obesity. 118,119 Furthermore, placentas of rhesus macaque dams fed a HFD exhibited reduced blood flow, increased calcification and risk for infarction. 66 A reduction in placental microvessel density has been observed as early as mid-gestation in a mouse model of dietinduced obesity.…”

Section: Pregravid Obesity and Placental Structurementioning

confidence: 99%

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Sureshchandra

Marshall

Messaoudi

2019

Journal of Leukocyte Biology

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Maternal pregravid obesity results in several adverse health outcomes during pregnancy, including increased risk of gestational diabetes, preeclampsia, placental abruption, and complications at delivery. Additionally, pregravid obesity and in utero exposure to high fat diet have been shown to have detrimental effects on fetal programming, predisposing the offspring to adverse cardiometabolic, endocrine, and neurodevelopmental outcomes. More recently, a deeper appreciation for the modulation of offspring immunity and infectious disease‐related outcomes by maternal pregravid obesity has emerged. This review will describe currently available animal models for studying the impact of maternal pregravid obesity on fetal immunity and review the data from clinical and animal model studies. We also examine the burden of pregravid obesity on the maternal–fetal interface and the link between placental and systemic inflammation. Finally, we discuss future studies needed to identify key mechanistic underpinnings that link maternal inflammatory changes and fetal cellular reprogramming events.

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Section: Pregravid Obesity and Placental Structurementioning

confidence: 99%

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Sureshchandra

Marshall

Messaoudi

2019

Journal of Leukocyte Biology

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“…The amount of copper transported across the placenta increases as gestation proceeds. The expression of the copper genes outlined in Figure 1 has been measured during pregnancy in a rat model (Lenartowicz et al, 2014). The pattern is different for the different genes, but tends to drop from about day 17 of gestation to term (21.5 days), thereafter increasing in the postnatal period (Lenartowicz et al, 2014).…”

Section: Figurementioning

confidence: 99%

“…The expression of the copper genes outlined in Figure 1 has been measured during pregnancy in a rat model (Lenartowicz et al, 2014). The pattern is different for the different genes, but tends to drop from about day 17 of gestation to term (21.5 days), thereafter increasing in the postnatal period (Lenartowicz et al, 2014). The expression in humans has not been determined, but, given that copper metabolism is similar in both species, it is not likely to be very different.…”

Section: Figurementioning

confidence: 99%

Scientific Opinion on Dietary Reference Values for copper

Products¹

2015

EFSA Journal

139

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Following a request from the European Commission, the EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) derived Dietary Reference Values (DRVs) for copper. Owing to the absence of appropriate biomarkers of copper status and the limitations of available balance studies, the Panel was unable to derive Average Requirements (ARs) and Population Reference Intakes (PRIs). Hence, Adequate Intakes (AIs) were defined based on mean observed intakes in several European Union (EU) countries, given that there is no evidence of overt copper deficiency in the European population. Data from balance studies were used as supportive evidence. For adults, AIs of 1.6 mg/day for men and 1.3 mg/day for women are proposed. For children, AIs are 0.7 mg/day for children aged 1 to < 3 years, 1 mg/day for children aged 3 to < 10 years, and 1.3 and 1.1 mg/day for boys and girls aged 10 to < 18 years, respectively. For infants aged 7-11 months, based on mean observed intakes in four EU countries, an AI of 0.4 mg/day is proposed, which is supported by upwards extrapolation of estimated copper intake in exclusively breast-fed infants. For pregnant women, an increment of 0.2 mg/day is estimated to cover the amount of copper deposited in the fetus and the placenta over the course of pregnancy and in anticipation of the needs for lactation, and for lactating women the same increment is estimated to cover the amount of copper secreted with breast milk. Thus, for pregnant and lactating women, the Panel derived an AI of 1.5 mg/day. Copper is an essential micronutrient required for electron transfer processes. It is a central component of many enzymes, including those involved in neurotransmitter synthesis, in energy metabolism and in collagen and elastin cross-linking.The main food group contributing to the copper intake of all population groups except infants is grains and grain-based products. Another important contributor to copper intake is the food group meat and meat products.Based on balance studies and other studies, the Panel considered that copper absorption from the diet is around 50 % for all age and life-stage groups.The primary site of copper absorption is the upper small intestine. Uptake is through a carrier protein, Ctr1, and once in the cell, the copper is directed towards its target via one of a series of chaperone proteins that ensure the metal is present in a non-toxic form. In the gut, the major pathway of transport into the portal circulation is via a Cu-ATPase, ATP7A. In the portal circulation, copper is bound to histidine, albumin or possibly transcuprein and transported to the liver, where it is incorporated into ceruloplasmin, which is then secreted into the systemic circulation. It is taken up into the liver through Ctr1 and, if it is not incorporated into ceruloplasmin, it is stored as metallothionein. Excess copper is excreted in bile after transport across the apical membrane of the hepatocytes via another ATPase, ATP7B. This copper is not reabsorbed. In humans, between 80 and 95 % of the copper in...

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“…In ETCM, blood serum copper status correlates with hepatic copper metabolism [110,111]. So, hepatic Cp-gene expression is low; the expression of Atp7b is practically absent.…”

Section: Ontogenetic Changes In Copper Metabolism In Mammalsmentioning

confidence: 99%

“…So, hepatic Cp-gene expression is low; the expression of Atp7b is practically absent. [108,110,111]. In intestinal, the transition from ETCM to ATCM occurs through increased abundance and altered localization of Ctr1, Atp7A, and Atp7B [110], as a result the mechanism controlling copper absorption is formed [113].…”

Section: Ontogenetic Changes In Copper Metabolism In Mammalsmentioning

confidence: 99%

Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin As a Nutritive Source of Copper

Puchkova¹,

Babich²,

Zatulovskaia³

et al. 2018

Preprint

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Copper, which can potentially be a highly toxic agent, is an essential nutrient due to its role as a co-factor for cuproenzymes and participation in signaling pathways. In mammals, the liver is a central organ that controls copper turnover throughout the body: copper absorption, distribution, and excretion. In ontogenesis, there are two types of copper metabolism: embryonic and adult, which maintain the balance of copper in each of these periods, respectively. In the liver cells, these types are characterized by specific expression patterns and activity levels of the genes encoding ceruloplasmin, which is the main extracellular ferroxidase and copper transporter and proteins mediating ceruloplasmin metalation. In newborns, the molecular-genetic mechanisms responsible for copper homeostasis and the ontogenetic switch from embryonic to adult copper metabolism are highly adapted to milk ceruloplasmin as a dietary source of copper. In the mammary gland cells, the level of ceruloplasmin gene expression and the alternative splicing of its pre-mRNA govern the amount of ceruloplasmin in milk, and thus, the amount of copper absorbed by the newborn is controlled. In the newborns, absorption, distribution, and accumulation copper are adapted to milk ceruloplasmin. In the newborns, which are not breast-fed at the early stages of postnatal development, the control for alimentary copper balance is absent. We tried to focus on the neonatal consequences of a violation of the balance of copper in the mother / newborn system. Although there is still much to be learned, the time to pay attention to this problem came because the neonatal misbalance of copper may provoke the development of copper related disorders for future life.

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Transcriptional regulation of copper metabolism genes in the liver of fetal and neonatal control and iron-deficient rats

Cited by 19 publications

References 69 publications

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Impact of pregravid obesity on maternal and fetal immunity: Fertile grounds for reprogramming

Scientific Opinion on Dietary Reference Values for copper

Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin As a Nutritive Source of Copper

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