scholarly journals Effect of dietary iron deficiency and overload on the expression of ZIP metal-ion transporters in rat liver

BioMetals ◽  
2011 ◽  
Vol 25 (1) ◽  
pp. 115-124 ◽  
Author(s):  
Hyeyoung Nam ◽  
Mitchell D. Knutson
Author(s):  
Abhishek Kulkarni ◽  
Monika Khade ◽  
Sharadha Arun ◽  
Pranesh Badami ◽  
G. Raja Krishna Kumar ◽  
...  

1994 ◽  
Vol 1188 (1-2) ◽  
pp. 46-52 ◽  
Author(s):  
Alberto Masini ◽  
Gianfranco Salvioli ◽  
Piero Cremonesi ◽  
Barbara Botti ◽  
Daniela Gallesi ◽  
...  

1992 ◽  
Vol 35 (1) ◽  
pp. 47-54 ◽  
Author(s):  
P. L. Ringeling ◽  
M. I. Cleton ◽  
M. I. E. Huijskes-Heins ◽  
W. C. de Bruijn ◽  
H. G. van Eijk
Keyword(s):  

2008 ◽  
Vol 36 (6) ◽  
pp. 1258-1261 ◽  
Author(s):  
Lorraine Gambling ◽  
Henriette S. Andersen ◽  
Harry J. McArdle

During development, the fetus is entirely dependent on the mother for its nutrient requirements. Subsequently, it is a period when both are vulnerable to changes in dietary supply, especially of those nutrients that are marginal under normal circumstances. In developed countries, this applies mainly to micronutrients. Even now, iron deficiency is a common disorder, especially in pregnancy. Similarly, copper intake in the U.K. population is rarely above adequate levels. It is now becoming clear that nutrient deficiencies during pregnancy can result in problems for the offspring, in both the short- and long-term. Early studies showed that lambs born to mothers on copper-deficient pastures developed ‘swayback’, with neurological and muscular symptoms that could not be reversed by postnatal supplementation. Our own findings have shown that prenatal iron deficiency results in increased postnatal blood pressure, even though the offspring have normal dietary iron levels from birth. These observations emphasize the importance of iron and copper in growth and development. Complicating the situation further is the fact that copper and iron are known to interact with each other in many ways, including absorption and intracellular transport. However, their interactions during the pregnancy appear to be more complex than during the non-pregnant state. In the present review, we examine the importance of these metals and their interactions, the consequences, both short- and long-term, of deficiency and consider some possible mechanisms whereby these effects may be generated.


2001 ◽  
Vol 204 (6) ◽  
pp. 1053-1061 ◽  
Author(s):  
A. Sacher ◽  
A. Cohen ◽  
N. Nelson

Transition metals are essential for many metabolic processes, and their homeostasis is crucial for life. Metal-ion transporters play a major role in maintaining the correct concentrations of the various metal ions in living cells. Little is known about the transport mechanism of metal ions by eukaryotic cells. Some insight has been gained from studies of the mammalian transporter DCT1 and the yeast transporter Smf1p by following the uptake of various metal ions and from electrophysiological experiments using Xenopus laevis oocytes injected with RNA copies (c-RNA) of the genes for these transporters. Both transporters catalyze the proton-dependent uptake of divalent cations accompanied by a ‘slippage’ phenomenon of different monovalent cations unique to each transporter. Here, we further characterize the transport activity of DCT1 and Smf1p, their substrate specificity and their transport properties. We observed that Zn(2+) is not transported through the membrane of Xenopus laevis oocytes by either transporter, even though it inhibits the transport of the other metal ions and enables protons to ‘slip’ through the DCT1 transporter. A special construct (Smf1p-s) was made to enhance Smf1p activity in oocytes to enable electrophysiological studies of Smf1p-s-expressing cells. 54Mn(2+) uptake by Smf1p-s was measured at various holding potentials. In the absence of Na(+) and at pH 5.5, metal-ion uptake was not affected by changes in negative holding potentials. Elevating the pH of the medium to 6.5 caused metal-ion uptake to be influenced by the holding potential: ion uptake increased when the potential was lowered. Na(+) inhibited metal-ion uptake in accordance with the elevation of the holding potential. A novel clutch mechanism of ion slippage that operates via continuously variable stoichiometry between the driving-force pathway (H(+)) and the transport pathway (divalent metal ions) is proposed. The possible physiological advantages of proton slippage through DCT1 and of Na(+) slippage through Smf1p are discussed.


PEDIATRICS ◽  
1971 ◽  
Vol 47 (4) ◽  
pp. 786-786
Author(s):  
L. J. Filer ◽  
Lewis A. Barness ◽  
Richard B. Goldbloom ◽  
Malcolm A. Holliday ◽  
Robert W. Miller ◽  
...  

In its recent statement on iron,1 the Committee on Nutrition emphasized the value of iron-fortified, proprietary milk formulas for the prevention of iron-deficiency anemia of infancy. Despite this recommendation, the most recent marketing information available to the Committee shows that more than 70% of the proprietary formulas currently prescribed by physicians do not contain added iron. The reasons for continuing routine use of formulas not fortified with iron are not entirely clear. One reason may be that some physicians still believe iron additives increase the incidence of feeding problems or gastrointestinal disturbances. There is no documented evidence that this is a significant problem. The Committee strongly recommends when proprietary formulas are prescribed that iron-supplemented formulas be used routinely as the standard–that is, that this be the rule rather than the exception. There seems to be little justification for continued general use of proprietary formulas not fortified with iron. The Committee is fully aware that only a small percentage of American infants are fed proprietary formulas after 6 months of age. Fluid whole milk (available in bottle or carton ) or evaporated milk, both of which contain only trace amounts of iron, are substituted at the time of greatest iron need and highest prevalence of iron-deficiency anemia. The infant's diet is usually deficient in iron, unless other foods are carefully selected to insure adequate iron intake. Since the major dietary component during infancy is milk, two courses of action should be taken: (1) Pediatricians and other health professionals should engage in a program of public education to convince American mothers to provide their infants with a source of dietary iron.


2022 ◽  
Author(s):  
Amanda K. Barks ◽  
Montana M. Beeson ◽  
Timothy C. Hallstrom ◽  
Michael K. Georgieff ◽  
Phu V. Tran

Iron deficiency (ID) during neurodevelopment is associated with lasting cognitive and socioemotional deficits, and increased risk for neuropsychiatric disease throughout the lifespan. These neurophenotypical changes are underlain by gene dysregulation in the brain that outlasts the period of ID; however, the mechanisms by which ID establishes and maintains gene expression changes are incompletely understood. The epigenetic modification 5-hydroxymethylcytosine (5hmC), or DNA hydroxymethylation, is one candidate mechanism because of its dependence on iron-containing TET enzymes. The aim of the present study was to determine the effect of fetal-neonatal ID on regional brain TET activity, Tet expression, and 5hmC in the developing rat hippocampus and cerebellum, and to determine whether changes are reversible with dietary iron treatment. Timed pregnant Sprague-Dawley rats were fed iron deficient diet (ID; 4 mg/kg Fe) from gestational day (G)2 to generate iron deficient anemic (IDA) offspring. Control dams were fed iron sufficient diet (IS; 200 mg/kg Fe). At postnatal day (P)7, a subset of ID-fed litters was randomized to IS diet, generating treated IDA (TIDA) offspring. At P15, hippocampus and cerebellum were isolated for subsequent analysis. TET activity was quantified by ELISA from nuclear proteins. Expression of Tet1, Tet2, and Tet3 was quantified by qPCR from total RNA. Global %5hmC was quantified by ELISA from genomic DNA. ID increased DNA hydroxymethylation (p=0.0105), with a corresponding increase in TET activity (p<0.0001) and Tet3 expression (p<0.0001) in the P15 hippocampus. In contrast, ID reduced TET activity (p=0.0016) in the P15 cerebellum, with minimal effect on DNA hydroxymethylation. Neonatal dietary iron treatment resulted in partial normalization of these changes in both brain regions. These results demonstrate that the TET/DNA hydroxymethylation system is disrupted by developmental ID in a brain region-specific manner. Differential regional disruption of this epigenetic system may contribute to the lasting neural circuit dysfunction and neurobehavioral dysfunction associated with developmental ID.


Sign in / Sign up

Export Citation Format

Share Document