THE CONSEQUENCES AND REVERSIBILITY OF CONGENITAL IRON DEFICIENCY ON THE AMOUNT OF NEURONS IN THE HIPPOCAMPAL AREA AND THE FATTY ACID COMPOSITION OF THE CEREBELLUM
Author
Gall, Marco
Term
4. term
Publication year
2011
Pages
38
Abstract
Baggrund: Jernmangel er den mest udbredte ernæringsforstyrrelse globalt, især hos gravide og børn. Medfødt jernmangel kan skade spædbørns kognitive og motoriske udvikling. Formål: Vi undersøgte, hvordan svær medfødt jernmangel påvirker antallet af neuroner i hippocampus og fedtsyresammensætningen i lillehjernen hos hanrotter (Wistar), og om jerntilskud givet i en tidlig kritisk periode (svarende til 3. trimester hos mennesker) kan modvirke disse effekter. Metode: Voksne hunrotter blev randomiseret til jernmangel eller kontrol. Jernmangel blev fremkaldt ved blodtapning (exsanguination) og en jernfattig diæt (<10 mg Fe/kg), mens kontrolgruppen fik standardfoder. Afkom fra jernmangel-dyr blev delt i to: et behandlingshold fik jerninjektioner (45 mg/kg iron isomaltoside 1000), og et hold fik saltvandsinjektioner og forblev jernmangelfuldt. Jernstatus blev fulgt med hæmatokritmålinger på flere tidspunkter. Omkring postnatal dag 85–90 blev motorik vurderet med et fodaftrykstest, og på dag 86–94 blev hjernen udtaget til måling af jern i mesencephalon, stereologisk optælling af hippocampus og fedtsyreanalyse af lillehjernen. Resultater: Jernmangelfulde dyr havde bredere gang end kontrol, men dette normaliseredes hos jernbehandlede dyr. I lillehjernen havde den jernbehandlede gruppe lavere docosahexaensyre (DHA, en omega-3-fedtsyre) og samlet mængde af flerumættede fedtsyrer (PUFA) end kontrol. Kontrolgruppen havde flere n-3 (omega-3) fedtsyrer end både jernmangel- og jernbehandlingsgruppen, mens jernmangelgruppen havde flere n-6 (omega-6) fedtsyrer end både jernbehandlede dyr og kontrol. I hippocampus’ gyrus dentatus (DG) var neuronantallet højere hos jernbehandlede dyr end hos ubehandlede med jernmangel. Konklusion: Jerntilskud med iron isomaltoside 1000 givet i den tidlige kritiske periode kan delvist vende de skadelige effekter af medfødt jernmangel. Motoriske problemer og lave blodværdier blev fuldt normaliseret, mens fedtsyresammensætningen i lillehjernen ikke blev helt genskabt. Tidlig jerntilførsel ser også ud til at øge antallet af neuroner i DG.
Background: Iron deficiency is the most common nutritional disorder worldwide, especially in pregnant women and children. Congenital iron deficiency can harm an infant’s cognitive and motor development. Objective: We examined how severe congenital iron deficiency affects neuron numbers in the hippocampus and fatty acid composition in the cerebellum of male Wistar rats, and whether iron given during a key early-life window (equivalent to the human third trimester) can counter these effects. Methods: Adult female rats were randomized to an iron-deficient or control diet. Iron deficiency was induced by exsanguination (bleeding) and an iron-poor diet (<10 mg Fe/kg); controls received standard chow. Offspring of iron-deficient dams were split into two groups: one received iron injections (45 mg/kg iron isomaltoside 1000), the other received saline and remained iron-deficient. Iron status was tracked by hematocrit at multiple time points. Around postnatal day 85–90, motor function was assessed with a footprint test; on days 86–94, brains were collected for mesencephalon iron measurement, stereological neuron counts in the hippocampus, and cerebellar fatty acid analysis. Results: Iron-deficient rats had a wider gait than controls, but iron-treated rats showed gait widths similar to controls. In the cerebellum, the iron-treated group had lower docosahexaenoic acid (DHA, an omega-3 fatty acid) and total polyunsaturated fatty acids (PUFAs) than controls. Controls had more n-3 (omega-3) fatty acids than both iron-deficient and iron-treated groups, and the untreated iron-deficient group had more n-6 (omega-6) fatty acids than both the iron-treated and control groups. In the hippocampal dentate gyrus (DG), neuron numbers were higher in iron-treated rats than in untreated iron-deficient rats. Conclusion: Iron isomaltoside 1000 given during the early window of opportunity can partially reverse the effects of congenital iron deficiency. Motor deficits and low blood values were fully corrected, but cerebellar lipid profiles did not fully normalize. Early iron also appears to increase neuron numbers in the DG.
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