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The effect of vitamin A deficiency on the biosynthesis of steroid hormones in rats.

ABSTRACT: 1. The synthesis, both in vivo and in vitro, of various steroid hormones in the adrenals, testes and ovaries of rats was compared at various stages of vitamin A deficiency with the corresponding pair-fed controls. 2. The enzymic conversion of the Delta(5)-3beta-hydroxy steroids into the corresponding Delta(4)-3-oxo steroids was significantly decreased in these tissues even at the mild-deficiency stage, further loss taking place on prolonging the deficiency. 3. In all three tissues the loss in the production of androstenedione from dehydroepiandrosterone could be reactivated in vitro by retinol or retinoic acid, but only at the mild stage of the deficiency. 4. Of the various lipoidal materials tried, retinal, retinol, retinoic acid, alpha-tocopherol acetate, menadione, calciferol, lecithin, palmitic acid and cholesterol, only retinol and retinoic acid restored the lost activity. 5. Intraperitoneal injection of retinal, retinol or retinoic acid into the deficient rats, 24hr. before they were killed, corrected the effect of the deficiency on this reaction. 6. Vitamin A deficiency markedly affected the synthesis of deoxycorticosterone and corticosterone from pregnenolone in the adrenals of rats, even at the mildly deficient stage, with further loss taking place at the acute stage; in vitro, retinol or retinoic acid could restore the loss at the mild-deficiency but not at the acute-deficiency stage. 7. The deficiency had no such effect on the synthesis of deoxycorticosterone from progesterone or of corticosterone from progesterone or deoxycorticosterone. 8. Compared with the pair-fed normals, the adrenals of deficient rats contained smaller amounts of deoxycorticosterone and corticosterone.

SUBMITTER: Juneja HS

PROVIDER: S-EPMC1264968 | biostudies-other | 1966 Apr

REPOSITORIES: biostudies-other

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Project description:In order to understand the molecular mechanism responsible for the therapeutic potential of vitamin D, we conducted an analysis of the liver transcriptome – a central place of metabolic changes. The experiment was carried out on adult female rats (about one year old), n=18, divided into three experimental subjects, receiving different doses of vitamin D for three months: group I - 0, group II - 1000 U/Kg, group III - 5000 U/Kg. After the experiment, the biochemical and haematological parameters of the blood were evaluated. RNA-seq was used to analyze the changes in the liver transcriptome, and Gene Set Enrichment Analysis (GSEA) was used to identify enrichments in gene expression profiles of experimental groups. qPCR was employed to evaluate the expression of several genes connected to cholesterol biosynthesis, metallothioneins, vitamin D metabolism and others. At the end of the experiment, 25(OH) vitamin D concentrations were as follows: group I: 29 ng/ml, group II 43: ng/ml, group III: 70 ng/mL. Considering blood parameters, we observed a lower platelet count (p<0,008) and significantly higher (p<0.02) number of WBC in rats supplemented with 1000 U/Kg than in rats from group III (5000 U/Kg), but no difference between rats from group I and III were detected in these parameters. Moreover, we noted a trend (p<0.06 ) in total cholesterol concentration, suggesting a linear decrease with increasing doses of vitamin D. RNA-seq analysis did not identify any differentially expressed genes with FDR<0.05 in any of the three comparisons. However, GSEA revealed significant activation of the number of processes and pathways. In the I vs III comparison, the most enriched were the genes from the “metallothionein, and TspO/MBR family” (Enrichment Score=8,170, FDR= 0.00006), the genes associated with “glyceraldehyde-3-phosphate dehydrogenase (NAD+) (phosphorylating) activity” (Enrichment Score=5.13, FDR<00049) and the genes associated with “Negative regulation of tumour necrosis factor production” (Enrichment score=1.26, FDR0.0064. qPCR analysis identified significant upregulation of Mt1, Mt2 and Orm1 genes in animals receiving high doses of vitamin D (p<0.025, p<0.025, p<0009, respectively). Moreover, significant downregulation of Srebp2 and Insig2 was observed in both experimental groups when compared to the control group (p<0.003, p<0.036, respectively). Our results support the potential of vitamin D supplementation in ameliorating oxidative stress, inflammation and high blood cholesterol and underlie the need for further studies aimed at identifying optimal vitamin D doses with therapeutic effects.

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The effect of vitamin A deficiency on the biosynthesis of steroid hormones in rats.

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