Perinatal thiamine deficiency-induced spontaneous abortion and pup-killing responses in rat dams

Bâ, Abdoulaye

doi:10.1179/1476830512y.0000000032

Cited by 10 publications

(11 citation statements)

References 83 publications

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“…The number of live fetuses per litter was consistently reduced (6.7 vs 11.2). In addition to spontaneous abortions, maternal pup-killing behavior and cannibalism was more frequently observed in deficient dams, as previously documented for thiamine deficiency [44]. …”

Section: Resultssupporting

confidence: 60%

Late Maternal Folate Supplementation Rescues from Methyl Donor Deficiency-Associated Brain Defects by Restoring Let-7 and miR-34 Pathways

et al. 2016

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The micronutrients folate and vitamin B12 are essential for the proper development of the central nervous system, and their deficiency during pregnancy has been associated with a wide range of disorders. They act as methyl donors in the one-carbon metabolism which critically influences epigenetic mechanisms. In order to depict further underlying mechanisms, we investigated the role of let-7 and miR-34, two microRNAs regulated by methylation, on a rat model of maternal deficiency. In several countries, public health policies recommend periconceptional supplementation with folic acid. However, the question about the duration and periodicity of supplementation remains. We therefore tested maternal supply (3 mg/kg/day) during the last third of gestation from embryonic days (E) 13 to 20. Methyl donor deficiency-related developmental disorders at E20, including cerebellar and interhemispheric suture defects and atrophy of selective cerebral layers, were associated with increased brain expression (by 2.5-fold) of let-7a and miR-34a, with subsequent downregulation of their regulatory targets such as Trim71 and Notch signaling partners, respectively. These processes could be reversed by siRNA strategy in differentiating neuroprogenitors lacking folate, with improvement of their morphological characteristics. While folic acid supplementation helped restoring the levels of let-7a and miR-34a and their downstream targets, it led to a reduction of structural and functional defects taking place during the perinatal period. Our data outline the potential role of let-7 and miR-34 and their related signaling pathways in the developmental defects following gestational methyl donor deficiency and support the likely usefulness of late folate supplementation in at risk women.Electronic supplementary materialThe online version of this article (doi:10.1007/s12035-016-0035-8) contains supplementary material, which is available to authorized users.

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Section: Resultssupporting

confidence: 60%

Late Maternal Folate Supplementation Rescues from Methyl Donor Deficiency-Associated Brain Defects by Restoring Let-7 and miR-34 Pathways

et al. 2016

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“…Some pups were cannibalised by their mothers within hours/days of birth, while others died with no signs of cannibalism on their carcass often weeks from birth. Strain and hormonal differences have been shown to influence pup-killing behaviour by female mice [38], [39]. Furthermore, females who give birth to deformed offspring were found more likely to consume their deformed offspring or dead young than their living healthy siblings [40], [41].…”

Section: Discussionmentioning

confidence: 99%

Foetal Loss and Enhanced Fertility Observed in Mice Treated with Zidovudine or Nevirapine

et al. 2014

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BackgroundHealth concerns for HIV-infected persons on antiretroviral therapy (ART) have moved from morbidity to the challenges of long-term ART. We investigated the effect of Zidovudine or Nevirapine on reproductive capacity across two mouse generations.MethodsA prospective mouse study with drugs administered through one spermatogenic cycle. Mouse groups (16 males and 10 females) were given Zidovudine or Nevirapine for 56 days. Males were mated to untreated virgin females to determine dominant lethal effects. Twenty females (10 treated and 10 untreated) mated with the treated males per dose and gave birth to the F1 generation. Parental mice were withdrawn from drugs for one spermatogenic cycle and mated to the same dams to ascertain if effects are reversible. The F1 generation were exposed for another 56 days and mated to produce the F2 generation.ResultsFoetal loss was indicated in the dominant lethal assay as early as four weeks into drug administration to the males. At the first mating of the parental generation to produce the F1 generation, births from 10 dams/dose when the ‘father-only’ was exposed to Zidovudine (10, 100 and 250 mg/kg) was 3, 2 and 1 while it was 7, 1 and 4 respectively when ‘both-parents’ were exposed. Similarly births from the parental generation first mating when the ‘father-only’ was exposed to Nevirapine (5, 50 and 150 mg/kg) was 2, 2 and 0 while it was 6, 5 and 9 respectively when ‘both-parents’ were exposed. However, fertility was not significantly different neither by dose nor by the parental exposure. The F1 mice mated to produce the F2 generation recorded only one birth.ConclusionThe dominant lethal analysis showed foetal loss occurred when the “fathers-only” were treated while fertility was enhanced when “both-parents” were on therapy at the time of mating.

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“…Periconceptional deficiencies of vitamin E, 21 thiamine, 82 and selenium 83 among others have been variably associated with spontaneous or recurrent pregnancy loss. Folate supplementation in an observational USA study of almost 16,000 women has been linked to a 20% lower risk of miscarriage (adjusted risk ratio [RR]: 0.80, 95% CI 0.71–0.90).…”

Section: Antenatal Effects Across the Lifespanmentioning

confidence: 99%

Micronutrient deficiencies in pregnancy worldwide: health effects and prevention

et al. 2016

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Micronutrients, vitamins and minerals accessible from the diet, are essential for biologic activity. Micronutrient status varies widely throughout pregnancy and across populations. Women in low-income countries often enter pregnancy malnourished, and the demands of gestation can exacerbate micronutrient deficiencies with health consequences to the fetus. Examples of efficacious single micronutrient interventions include folic acid to prevent neural tube defects, iodine to prevent cretinism, zinc to reduce of preterm birth, and iron to reduce the risk of low birth weight. Folic acid and vitamin D might also increase birth weight. While extensive mechanism and association research links antenatal multiple micronutrients to plausible materno-fetal health advantages, hypothesized benefits have often been absent, minimal or unexpected in trials. These findings suggest a role for population context in determining health responses and extensive gaps in knowledge. Multiple micronutrient supplements reduce risks of being born low birth weight, small for gestational age or stillborn in undernourished settings, and justify micronutrient interventions with antenatal care. Measurable health effects of gestational micronutrient exposure may persist into childhood but few data exists on potential long-term benefits. In this Review, we discuss micronutrient intake recommendations, risks and consequences of deficiencies, and the effects of interventions with a particular emphasis on offspring.

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Perinatal thiamine deficiency-induced spontaneous abortion and pup-killing responses in rat dams

Cited by 10 publications

References 83 publications

Late Maternal Folate Supplementation Rescues from Methyl Donor Deficiency-Associated Brain Defects by Restoring Let-7 and miR-34 Pathways

Late Maternal Folate Supplementation Rescues from Methyl Donor Deficiency-Associated Brain Defects by Restoring Let-7 and miR-34 Pathways

Foetal Loss and Enhanced Fertility Observed in Mice Treated with Zidovudine or Nevirapine

Micronutrient deficiencies in pregnancy worldwide: health effects and prevention

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