Characterization of iron deficiency and the dietary iron requirement of fingerling channel catfish

Aquaculture ◽  
1986 ◽  
Vol 52 (3) ◽  
pp. 191-198 ◽  
Author(s):  
Delbert M. Gatlin ◽  
Robert P. Wilson
2019 ◽  
Vol 149 (3) ◽  
pp. 366-371 ◽  
Author(s):  
Santu Ghosh ◽  
Srishti Sinha ◽  
Tinku Thomas ◽  
Harshpal S Sachdev ◽  
Anura V Kurpad

ABSTRACT Anemia in Indian women continues to be highly prevalent, and is thought to be due to low dietary iron content. The high risk of dietary iron deficiency is based on the Indian Council of Medical Research recommendation of 21 mg/d, but there is a need for a secure and transparent determination of the Estimated Average Requirement (EAR) of iron in this population. In nonpregnant, nonlactating women of reproductive age (WRA), the EAR of iron was determined to be 15 mg/d. Applying this value to daily iron intakes among WRA in nationally representative Indian state–based data showed that the median risk of dietary iron deficiency was lower than previously thought (65%; IQR: 48–78%), with considerable heterogeneity between states (range: 25–93%). However, in a validation, this risk matched the risk of iron deficiency as defined by blood biomarkers in a recently completed survey. When the risk of dietary iron deficiency was modelled for an increase in iron intake through food fortification of a single dietary staple, that provided 10 mg/d, the median risk reduced substantially (from 65% to 20%), and it virtually disappeared when supplementary iron intakes through the national iron supplementation program were considered. The risk of exceeding the tolerable upper level (TUL) of intake of iron remains low in the population when receiving fortification of 10 mg/d, but is much higher if they consume greater amounts of iron through supplements (range: 0–54%). This newly and transparently defined Indian EAR of iron should be used to evaluate, with precision, the benefits and risks of iron fortification and supplementation policies.


2012 ◽  
Vol 36 (2) ◽  
pp. 314
Author(s):  
Jian-feng LU ◽  
Chang-wei MENG ◽  
Jin LI ◽  
Zi-hui GONG ◽  
Lin LIN ◽  
...  

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 ◽  
...  

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.


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.


2014 ◽  
Vol 75 ◽  
pp. 89-95 ◽  
Author(s):  
Lili Yin ◽  
Yi Wang ◽  
Mudan Yuan ◽  
Xinzhong Zhang ◽  
Xuefeng Xu ◽  
...  

Author(s):  
RABAB HASSAN ELSHAIKH ◽  
SANAA ELFATIH HUSSEIN

Thalassemia is common inherited disorder among humans, and they represent a major public health problem in many areas of the world. The study aimed to the measurement of hematological characterization of beta-thalassemia in Sudanese patients. Blood samples from 61 beta-thalassemic patients were collected after written consent form obtained from all participants. The frequency of adults (>18 years) was 45 (73.8%) and children’s (<18 years) was 16 (26.2%); the frequency of male was 27 (44.3%) and 34 were female (55.7%). Hemoglobin estimation and red cell indices were carried out using the automatic blood cell counter Sysmex K × 21N. The results showed that Hb and RBCs indices were varied between mild to moderate and severe decreasing, hemoglobin concentration (Hb) with the mean value of 9.6 g/dL, with minimum value of 6.1 g/dl and maximum of 11.9 g/dl, while RBCs were increased in all patients, mean value 5.2 c/l, mean corpuscular volume mean was 58.9 fl, hematocrit was 30.4, mean corpuscular hemoglobin (MCH) 18.8 pg, mean corpuscular hemoglobin concentration (MCHC) was 31.7pg, and RDW was 18.8%. The method used for hemoglobin electrophoresis was capillary electrophoresis, Hb pattern shows increased HbA2 and HbF, the mean of HbA is 78.3%, HbF is 2.3%, and HbA2 is 6.5% with the min. value of 3.6% and max. of 12.2%. While the mean of serum iron was 82.75 μg/dl, 7 patients showed low level, 19 high level, and 35 were normal level. Comparison of hematological analysis (HbA2) in thalassemic patients coexisted with iron deficiency and without result was insignificant difference (p=0.645), this result disagrees with references that say iron deficiency masking HbA2. Nevertheless, the association between HbA2 and HbF revealed a statistically significant difference (p<0.013) and HbA2 with Hb was insignificant (p=0.260).


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