An iron-deficient diet stimulates the onset of the hepatitis due to hepatic copper deposition in the Long-Evans Cinnamon (LEC) rat

1999 ◽  
Vol 73 (7) ◽  
pp. 353-358 ◽  
Author(s):  
Naoki Sugawara ◽  
Chieko Sugawara
Keyword(s):  
Copper Deposition ◽  
Deficient Diet ◽  
Hepatic Copper ◽  
Iron Deficient ◽  
Long Evans

Inverse relationship of hepatic copper and iron concentrations in rats fed deficient diets

1968 ◽  
Vol 46 (3) ◽  
pp. 267-271 ◽  
Author(s):  
T. L. Sourkes ◽  
K. Lloyd ◽  
H. Birnbaum
Keyword(s):  
Corn Starch ◽  
Milk Powder ◽  
Skim Milk ◽  
Young Male ◽  
Skim Milk Powder ◽  
Albino Rats ◽  
Cupric Sulfate ◽  
Deficient Diet ◽  
Hepatic Copper ◽  
Iron Deficient

Young male albino rats were fed a diet based upon equal parts of skim milk powder and corn starch. Dietary supplements included cupric sulfate, ferrous sulfate, both salts, or neither. Rats consuming the iron-deficient diet accumulated high concentrations of copper in the liver, a process that became evident only after 7–8 weeks. The rats fed the copper-deficient diet accumulated excessive amounts of iron, beginning much earlier. The hepatic concentrations of copper and iron in these experiments were inversely correlated (P < 0.01) in a complex relationship.

Hepatic Copper Accumulation Induces DNA Strand Breaks in the Liver Cells of Long-Evans Cinnamon Strain Rats

2000 ◽  
Vol 276 (1) ◽  
pp. 174-178 ◽  
Author(s):  
Masanobu Hayashi ◽  
Tomoko Kuge ◽  
Daiji Endoh ◽  
Kenji Nakayama ◽  
Jiro Arikawa ◽  
...  
Keyword(s):  
Dna Strand Breaks ◽  
Liver Cells ◽  
Copper Accumulation ◽  
Strand Breaks ◽  
Hepatic Copper ◽  
Long Evans ◽  
Dna Strand

Developmental iron deficiency dysregulates TET activity and DNA hydroxymethylation in the rat hippocampus and cerebellum

2022 ◽  
Author(s):  
Amanda K. Barks ◽  
Montana M. Beeson ◽  
Timothy C. Hallstrom ◽  
Michael K. Georgieff ◽  
Phu V. Tran
Keyword(s):  
Iron Deficiency ◽  
Neural Circuit ◽  
Epigenetic Modification ◽  
Rat Hippocampus ◽  
Dietary Iron ◽  
Deficient Diet ◽  
Dna Hydroxymethylation ◽  
Iron Treatment ◽  
Iron Deficient ◽  
Increased Risk

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.

scholarly journals The Treatment of Iron Deficiency Anemia

Blood ◽  
1955 ◽  
Vol 10 (6) ◽  
pp. 567-581 ◽  
Author(s):  
DANIEL H. COLEMAN ◽  
ALEXANDER R. STEVENS ◽  
CLEMENT A. FINCH
Keyword(s):  
Iron Deficiency ◽  
Gastrointestinal Symptoms ◽  
The Body ◽  
Deficiency Anemia ◽  
Deficient Diet ◽  
Significant Group ◽  
Body Iron ◽  
Iron Stores ◽  
Iron Deficient ◽  
Full Complement

Abstract In the normal individual the amount of iron absorbed and lost from the body each day is exceedingly small. There are certain periods during life when body iron requirements are increased; the most important of these is infancy. Here, existing iron stores are rapidly depleted, and a deficient diet can soon produce iron deficiency. Once a full complement of body iron has been accrued, the adult is independent of iron intake and becomes iron deficient only through blood loss. In the production of iron deficiency, iron stores are exhausted before anemia appears. If any question in diagnosis from usual laboratory tests exists, the direct. examination of marrow for hemosiderin will establish the diagnosis. It is of obvious importance to confirm the diagnosis by specific therapy and to determine the cause of the iron depletion. Response to oral iron is highly predictable and failure of response usually in dictates a mistaken diagnosis. In a small but significant group of patients, either unable to take iron because of gastrointestinal symptoms, unable to absorb iron, or in need of iron reserves, parenteral administration of iron has distinct advantages. The saccharated oxide of iron is an effective preparation for this purpose.

Iron restriction improves type 2 diabetes mellitus in Otsuka Long-Evans Tokushima fatty rats

2010 ◽  
Vol 298 (6) ◽  
pp. E1140-E1149 ◽  
Author(s):  
Yukiko Minamiyama ◽  
Shigekazu Takemura ◽  
Shintaro Kodai ◽  
Hiroji Shinkawa ◽  
Takuma Tsukioka ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Signal Pathways ◽  
Peroxisome Proliferator ◽  
Iron Depletion ◽  
Ferritin Concentration ◽  
Iron Restriction ◽  
Oletf Rats ◽  
Iron Deficient ◽  
Long Evans

Accumulating evidence suggests that alcohol, hepatitis C virus infection, steatosis with obesity, and insulin resistance are accompanied by iron overload states. Phlebotomy and oral iron chelators are effective treatments for these conditions and for hemochromatosis. However, the mechanisms by which iron depletion improves clinical factors remain unclear. We examined the effect of iron depletion in a model of type 2 diabetes, Otsuka Long-Evans Tokushima Fatty (OLETF) rats. Age-matched Long-Evans Tokushima Otsuka (LETO) rats were used as controls for all experiments. Iron restriction was performed by eliminating iron in the diet from 15 wk of age or by phlebotomy. Phlebotomy was commenced at 29 wk of age by removing 4 and 3 ml of blood from the tail vein every week in OLETF and LETO rats, respectively. Rats were euthanized at 43 wk of age, and detailed analyses were performed. The plasma ferritin concentration was markedly higher in OLETF rats and decreased in iron-deficient (ID) diet and phlebotomy rats. Hemoglobin A1c (Hb A1c) was decreased significantly in OLETF rats fed the ID diet and in the phlebotomy group. Increased levels of triglycerides, glucose, free fatty acids, and total cholesterol were found in ID OLETF rats. Plasma, liver, and pancreas lipid peroxidation and hepatic superoxide production decreased in both groups. Pancreatic fibrosis and insulin levels improved in both groups of OLETF rats. Pancreatic levels of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) ligands and hypoxia-inducible factor (HIF)-1α were decreased significantly in OLETF rats. These factors were normalized in both rats fed ID and phlebotomy groups of OLETF rats. In conclusion, iron depletion improved diabetic complications by inhibition of oxidative stress and TGFβ signal pathways and the maintenance of pancreatic PPARβ/δ and HIF-1α pathways.

Relationship between intestinal iron-transporter expression, hepatic hepcidin levels and the control of iron absorption

2002 ◽  
Vol 30 (4) ◽  
pp. 724-726 ◽  
Author(s):  
G.J. Anderson ◽  
D. M. Frazer ◽  
S.J. Wilkins ◽  
E. M. Becker ◽  
K. N. Millard ◽  
...  
Keyword(s):  
Iron Transport ◽  
Iron Absorption ◽  
Negative Regulator ◽  
Deficient Diet ◽  
Divalent Metal Transporter 1 ◽  
Intestinal Iron Absorption ◽  
Divalent Metal Transporter ◽  
Hepcidin Expression ◽  
Iron Deficient ◽  
Transport Molecules

Hepcidin is an anti-microbial peptide predicted to be involved in the regulation of intestinal iron absorption. We have examined the relationship between the expression of hepcidin in the liver and the expression of the iron-transport molecules divalent-metal transporter 1, duodenal cytochrome b, hephaestin and Ireg1 in the duodenum of rats switched from an iron-replete to an iron-deficient diet or treated to induce an acute phase response. In each case, elevated hepcidin expression correlated with reduced iron absorption and depressed levels of iron-transport molecules. These data are consistent with hepcidin playing a role as a negative regulator of intestinal iron absorption.

Iron Absorption: The Effect of an Iron-Deficient Diet

Science ◽  
1964 ◽  
Vol 144 (3621) ◽  
pp. 1015-1016 ◽  
Author(s):  
S. Pollack ◽  
R. M. Kaufman ◽  
W. H. Crosby
Keyword(s):  
Iron Absorption ◽  
Deficient Diet ◽  
Iron Deficient

The Response of Larvae of the Large White Butterfly (Pieris brassicae (L.)) to Diets of Mineral-deficient Leaves

1957 ◽  
Vol 48 (1) ◽  
pp. 229-242 ◽  
Author(s):  
M. Delia Allen ◽  
Ireson W. Selman
Keyword(s):  
Growth Rate ◽  
Relative Growth Rate ◽  
Larval Mortality ◽  
Pieris Brassicae ◽  
Larval Life ◽  
Large White ◽  
Deficient Diet ◽  
Relative Growth ◽  
Larval Instars ◽  
Iron Deficient

When larvae of Pieris brassicae (L.) were fed on leaves of plants showing symptoms of deficiency of nitrogen, phosphorus, potassium or iron, some or all of the following effects were recorded in each experiment: —Reduction of larval weight (deficiency of (1) N, P, K throughout larval life, (2) Fe from time of hatching, from sixth day and for the last two larval instars).Reduction of relative growth rate (deficiency of (1) N throughout larval life, (2) Fe from time of hatching, from sixth day and for last two larval instars).Increased larval mortality (deficiency of N, Fe from time of hatching).Delayed pupation (deficiency of (1) N, P, K throughout larval life, (2) Fe from time of hatching, from sixth day and for the last two larval instars).The more detailed experiments with iron-deficient diet showed that similar effects were produced at whatever stage of larval development it was first supplied.Larvae fed on iron-deficient leaves from the time of hatching appeared to have received a severe initial check to growth, but this was followed by some degree of recovery so that they showed a higher relative growth rate, a few days later, than larvae given the same diet six days after hatching.Preliminary trials were made on the effects of the addition to diets of iron-deficient leaves of various nutrient substances sprayed on to them. No markedly beneficial results were noted.

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