Growth in Iron-Deficient Rats

Beard, John L.; Zhan, Cenchen S.; Brigham, Dale E.

doi:10.3181/00379727-209-43879

Cited by 24 publications

(19 citation statements)

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“…This is consistent with several previous studies reporting decreased food intake associated with poor growth in rats suffering from ID anaemia [12,28-30]. However, previous depletion studies showed that severe ID decreased relative weight gain (g weight gain per g food intake) [12,28], while in the current study, relative weight gain was the same in rats repleted with Fe and remaining ID. Since neurotransmitters, including DA and 5-HT, are involved in the regulation of food intake [31], it is possible that the reduced food intake of ID rats is related to alterations in monoaminergic neurotransmission.…”

Section: Discussionsupporting

confidence: 93%

Providing male rats deficient in iron and n-3 fatty acids with iron and alpha-linolenic acid alone affects brain serotonin and cognition differently from combined provision

2014

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BackgroundWe recently showed that a combined deficiency of iron (ID) and n-3 fatty acids (n-3 FAD) in rats disrupts brain monoamine metabolism and produces greater memory deficits than ID or n-3 FAD alone. Providing these double-deficient rats with either iron (Fe) or preformed docosahexaenoic acid (DHA)/eicosapentaenoic acid (EPA) alone affected brain monoamine pathways differently from combined repletion and even exacerbated cognitive deficits associated with double-deficiency. Iron is a co-factor of the enzymes responsible for the conversion of alpha-linolenic acid (ALA) to EPA and DHA, thus, the provision of ALA with Fe might be more effective in restoring brain EPA and DHA and improving cognition in double-deficient rats than ALA alone.MethodsIn this study we examined whether providing double-deficient rats with ALA and Fe, alone or in combination, can correct deficits in monoamine metabolism and cognition associated with double-deficiency. Using a 2 × 2 design, male rats with concurrent ID and n-3 FAD were fed an Fe + ALA, Fe + n-3 FAD, ID + ALA, or ID + n-3 FAD diet for 5 weeks (postnatal day 56–91). Biochemical measures, and spatial working and reference memory (using the Morris water maze) were compared to age-matched controls.ResultsIn the hippocampus, we found a significant Fe × ALA interaction on DHA: Compared to the group receiving ALA alone, DHA was significantly higher in the Fe + ALA group. In the brain, we found significant antagonistic Fe × ALA interactions on serotonin concentrations. Provision of ALA alone impaired working memory compared with age-matched controls, while in the reference memory task ALA provided with Fe significantly improved performance.ConclusionThese results indicate that providing either iron or ALA alone to double-deficient rats affects serotonin pathways and cognitive performance differently from combined provision. This may be partly explained by the enhancing effect of Fe on the conversion of ALA to EPA and DHA.

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Section: Discussionsupporting

confidence: 93%

Providing male rats deficient in iron and n-3 fatty acids with iron and alpha-linolenic acid alone affects brain serotonin and cognition differently from combined provision

2014

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“…Growth retardation is not a common finding unless IDA is severe; retarded growth linked to altered metabolism has been demonstrated in rodent models [38,3] and stunting is found in connection with anemia in generally malnourished populations [34]. A smaller head width was detected in the prenatally deprived group, but head circumferences did not differ, suggesting a conformational rather than growth related source of the head width difference.…”

Section: Discussionmentioning

confidence: 89%

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys

Golub

Hogrefe

Germann

et al. 2006

Neurotoxicology and Teratology

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Human studies have shown that iron deficiency and iron deficiency anemia in infants are associated with behavioral impairment, but the periods of brain development most susceptible to iron deficiency have not been established. In the present study, rhesus monkeys were deprived of iron by dietary iron restriction during prenatal (n = 14, 10 μg Fe/g diet) or early postnatal (n = 12, 1.5 mg Fe/L formula) brain development and compared to controls (n = 12, 100 μg Fe/g diet, 12 mg Fe/L formula) in behavioral evaluations conducted during the first four months of life in the nonhuman primate nursery. Iron deficiency anemia was detected in the pregnant dams in the third trimester and compromised iron status was seen in the prenatally iron-deprived infants at birth, but no iron deficiency was seen in either the prenatally or postnatally iron-deprived infants during the period of behavioral evaluation. Neither prenatal nor postnatal iron deprivation led to significant delays in growth, or gross or fine motor development. Prenatally deprived infants demonstrated a 20% reduced spontaneous activity level, lower inhibitory response to novel environments, and more changes from one behavior to another in weekly observation sessions. Postnatally deprived infants demonstrated poorer performance of an object concept task, and greater emotionality relative to controls. This study indicates that different syndromes of behavioral effects are associated with prenatal and postnatal iron deprivation in rhesus monkey infants and that these effects can occur in the absence of concurrent iron deficiency as reflected in hematological measures.

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“…The control group received the AIN 93-G diet containing 50 mg elemental iron per kg diet (13,14). The anemic group was fed the same diet, but containing less than 5 mg elemental iron per kg diet.…”

Section: Methodsmentioning

confidence: 99%

“…Feed efficiency was calculated by dividing weight gain by food consumption during the study period (13). Hemoglobin and hematocrit were determined at 0, 2, 4, and 6 weeks.…”

Section: Methodsmentioning

confidence: 99%

Morphological and functional alterations of the intestine of rats with iron-deficiency anemia

Wayhs

Patricio

Amâncio

et al. 2004

Braz J Med Biol Res

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The present study was designed to assess the intestinal absorption of D-xylose and jejunal morphometry in rats with iron-deficiency anemia. Male Wistar rats were randomly divided into a control group (diet containing 50 mg Fe/kg, N = 12) and an anemic group (diet containing <5 mg Fe/kg, N = 12). The animals were housed in individual metabolic cages and deionized water and diet were provided ad libitum for 6 weeks. Hemoglobin and hematocrit were determined at 0, 2, 4, and 6 weeks. At the end of the study the rats were submitted to a D-xylose absorption test (50 mg/100 g body weight) and sacrificed and a jejunal specimen was obtained for morphometric study. At the end of the study the hemoglobin and hematocrit of the anemic rats (8.7 ± 0.9 g/dl and 34.1 ± 2.9%, respectively) were significantly (P < 0.05) lower than those of the controls (13.9 ± 1.4 g/dl and 47.1 ± 1.5%, respectively). There was no statistical difference in D-xylose absorption between the anemic (46.5 ± 7.4%) and control (43.4 ± 9.0%) groups. The anemic animals presented statistically greater villus height (445.3 ± 36.8 µm), mucosal thickness (614.3 ± 56.3 µm) and epithelial surface (5063.0 ± 658.6 µm) than control (371.8 ± 34.3, 526.7 ± 62.3 and 4401.2 ± 704.4 µm, respectively; P < 0.05). The increase in jejunum villus height, mucosal thickness and epithelial surface in rats with iron-deficiency anemia suggests a compensatory intestinal mechanism to increase intestinal iron absorption.

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Growth in Iron-Deficient Rats

Cited by 24 publications

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Providing male rats deficient in iron and n-3 fatty acids with iron and alpha-linolenic acid alone affects brain serotonin and cognition differently from combined provision

Providing male rats deficient in iron and n-3 fatty acids with iron and alpha-linolenic acid alone affects brain serotonin and cognition differently from combined provision

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys

Morphological and functional alterations of the intestine of rats with iron-deficiency anemia

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