Influences of Maternal B12 and Methionine Intake during Gestation and Lactation on Testicular Development of Offspring in Rats

Yamada, Keiko; Maeda, Nozomi; Noguchi, Junko; Yamada, Hideaki; Morinaga, Emi; Yatake, Hitomi; Yamamoto, Yuji; Tadokoro, Tadahiro; Kawata, Toshitsugu

doi:10.3177/jnsv.59.238

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…These tcn2 Ϫ/Ϫ fish demonstrate no obvious developmental or behavioral phenotypes, which is inconsistent with models of vitamin B 12 deficiency in mammals (as reviewed in Ref. 22) (24). As cobalamin remains an essential enzymatic cofactor in fish (29), the benign effects of tcn2 knockout strongly suggests a compensatory, as yet undescribed, system of cobalamin transport in zebrafish.…”

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confidence: 95%

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Functional and phylogenetic characterization of noncanonical vitamin B12–binding proteins in zebrafish suggests involvement in cobalamin transport

Benoit

Stanton

Tartanian

et al. 2018

Journal of Biological Chemistry

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Edited by Ruma Banerjee In humans, transport of food-derived cobalamin (vitamin B 12) from the digestive system into the bloodstream involves three paralogous proteins: transcobalamin (TC), haptocorrin (HC), and intrinsic factor (IF). Each of these proteins contains two domains, an ␣-domain and a ␤-domain, which together form a cleft in which cobalamin binds. Zebrafish (Danio rerio) are thought to possess only a single cobalamin transport protein, referred to as Tcn2, which is a transcobalamin homolog. Here, we used CRISPR/Cas9 mutagenesis to create null alleles of tcn2 in zebrafish. Fish homozygous for tcn2-null alleles were viable and exhibited no obvious developmentally or behaviorally abnormal phenotypes. For this reason, we hypothesized that previously unidentified cobalamin-carrier proteins encoded in the zebrafish genome may provide an additional pathway for cobalamin transport. We identified genes predicted to code for two such proteins, Tcn-beta-a (Tcnba) and Tcn-beta-b (Tcnbb), which differ from all previously characterized cobalamin transport proteins as they lack the ␣-domain. These ␤-domainonly proteins are representative of an undescribed class of cobalamin-carrier proteins that are highly conserved throughout the ray-finned fishes. We observed that the genes encoding the three cobalamin transport homologs, tcn2, tcnba, and tcnbb, are expressed in unique spatial and temporal patterns in the developing zebrafish. Moreover, exogenously expressed recombinant Tcnba and Tcnbb bound cobalamin with high affinity, comparable with binding by full-length Tcn2. Taken together, our results suggest that this noncanonical protein structure has evolved to fully function as a cobalamin-carrier protein, thereby allowing for a compensatory cobalamin transport mechanism in the tcn2 ؊/؊ zebrafish. Vitamin B 12 , also referred to as cobalamin, is a micronutrient that acts as a cofactor for two enzymes: methionine synthase, This article contains Figs. S1-S4 and Table S1.

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“…Although vitamin B 12 deficiency is a serious worldwide health issue, nonclinical research has been primarily limited to mammalian models (22)(23)(24)(25)(26)(27)(28). Zebrafish (Danio rerio) are a potentially powerful model system with which to study vitamin B 12 metabolism and biology.…”

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confidence: 99%

Functional and phylogenetic characterization of noncanonical vitamin B12–binding proteins in zebrafish suggests involvement in cobalamin transport

Benoit

Stanton

Tartanian

et al. 2018

Journal of Biological Chemistry

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“…Micronutrients such as many vitamins regulate the expression of key genes involved in growth and proliferation and in the functional attributes of specific organs [ 3 ]. The literature points out that the micronutrient imbalance may also affect the development of the androgen-dependent organs, such as penis [ 4 ].…”

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confidence: 99%

Effects of Vitamin D Restricted Diet Administered during Perinatal and Postnatal Periods on the Penis of Wistar Rats

Fernandes-Lima

Gregório

Nascimento

et al. 2018

BioMed Research International

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Vitamin D deficiency is common in pregnant women and infants. The present study aimed to investigate the effects of vitamin D restricted diet on the Wistar rats offspring penis morphology. Mother rats received either standard diet (SC) or vitamin D restricted (VitD) diet. At birth, offspring were divided into SC/SC (from SC mothers, fed with SC diet) and VitD/VitD (from VitD mothers, fed with VitD diet). After euthanasia the penises were processed for histomorphometric analysis. The VitD/VitD offspring displayed metabolic changes and reduction in the cross-sectional area of the penis, corpus cavernosum, tunica albuginea, and increased area of the corpus spongiosum. The connective tissue, smooth muscle, and cell proliferation percentages were greater in the corpus cavernosum and corpus spongiosum in the VitD/VitD offspring. The percentages of sinusoidal spaces and elastic fibers in the corpus cavernosum decreased. The elastic fibers in the tunica albuginea of the corpus spongiosum in the VitD/VitD offspring were reduced. Vitamin D restriction during perinatal and postnatal periods induced metabolic and structural changes and represented important risk factors for erectile dysfunction in the penis of the adult offspring. These findings suggest that vitamin D is an important micronutrient in maintaining the cytoarchitecture of the penis.

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Developmental origins of male subfertility: role of infection, inflammation, and environmental factors

et al. 2016

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Male gamete development begins with the specification of primordial cells in the epiblast of the early embryo and is not complete until spermatozoa mature in the epididymis of adult males. This protracted developmental process involves extensive alteration of the paternal germline epigenome. Initially, epigenetic reprogramming in fetal germ cells results in removal of most DNA methylation, including parent-specific epigenetic information. The germ cells then establish sex-specific epigenetic information through de novo methylation and undergo spermatogenesis. Chromatin in haploid germ cells is repackaged into protamines during spermiogenesis, providing further widespread epigenetic reorganization. Finally, after fertilization, epigenetic reprogramming in the preimplantation embryo is necessary for regaining totipotency. These events provide substantial windows during which epigenetic errors either may be corrected or may occur in the germline. There is now increasing evidence that environmental factors such as exposure to toxicants, the parents' and individual's diet, and even infectious and inflammatory events in the male reproductive tract may influence epigenetic reprogramming. This, together with other damage inflicted on the germline chromatin, may result in negative consequences for fertility and health. Large epidemiological birth cohort studies have yielded insight into possible causative environmental factors. Together with experimental animal studies, a clearer view of environmental impacts on fetal development and their intergenerational and even transgenerational effects on reproductive health has emerged and is reviewed in this article.

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Influences of Maternal B12 and Methionine Intake during Gestation and Lactation on Testicular Development of Offspring in Rats

Cited by 6 publications

References 19 publications

Functional and phylogenetic characterization of noncanonical vitamin B12–binding proteins in zebrafish suggests involvement in cobalamin transport

Functional and phylogenetic characterization of noncanonical vitamin B12–binding proteins in zebrafish suggests involvement in cobalamin transport

Effects of Vitamin D Restricted Diet Administered during Perinatal and Postnatal Periods on the Penis of Wistar Rats

Developmental origins of male subfertility: role of infection, inflammation, and environmental factors

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