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Genomic actions of 1,25-dihydroxyvitamin D3 on insulin receptor gene expression, insulin receptor number and insulin activity in the kidney, liver and adipose tissue of streptozotocin-induced diabetic rats.

Calle C, Maestro B, García-Arencibia M - BMC Mol. Biol. (2008)

Bottom Line: These effects were accompanied by a normalization of the number of insulin receptors without altering receptor affinity but improving the insulin response to glucose transport in adipocytes from these diabetic animals.Moreover, a computer search in the rat insulin receptor promoter revealed the existence of two candidate vitamin D response element (VDRE) sequences located at -256/-219 bp and -653/-620 bp, the first overlapped by three and the second by four AP-2-like sites. these genomic actions of 1,25D3 could represent beneficial effects associated with the amelioration of diabetes via mechanisms that possibly involve direct transcriptional activation of the rat insulin receptor gene.The candidate VDREs identified may respond to 1,25D3 via activation of the vitamin D receptor, although this remains to be investigated.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, School of Medicine, Complutense University, 28040-Madrid, Spain. consuelo@med.ucm.es

ABSTRACT

Background: this study set out to examine the effects of the treatment with 1,25-dihydroxyvitamin D3 (1,25D3) [150 IU/Kg (3.75 microg/Kg) one a day, for 15 days] to non-diabetic rats and in rats rendered diabetic by a single injection of streptozotocin [65 mg/kg].

Results: treatment with 1,25D3 to non-diabetic rats did not affect the biochemical parameters measured in the plasma and urine of these animals. Likewise, insulin receptor expression in the kidney, liver, or adipose tissue and insulin-stimulated glucose transport in adipocytes from these animals were not affected either. Treatment with 1,25D3 to streptozotocin-induced diabetic rats did not correct the hyperglycemia, hypoinsulinemia, glycosuria or ketonemia induced by the diabetes, although it partially reversed the over-expression of the insulin receptor gene in the liver and adipose tissue, without altering the normal expression of this gene in the kidney. These effects were accompanied by a normalization of the number of insulin receptors without altering receptor affinity but improving the insulin response to glucose transport in adipocytes from these diabetic animals. Moreover, a computer search in the rat insulin receptor promoter revealed the existence of two candidate vitamin D response element (VDRE) sequences located at -256/-219 bp and -653/-620 bp, the first overlapped by three and the second by four AP-2-like sites.

Conclusion: these genomic actions of 1,25D3 could represent beneficial effects associated with the amelioration of diabetes via mechanisms that possibly involve direct transcriptional activation of the rat insulin receptor gene. The candidate VDREs identified may respond to 1,25D3 via activation of the vitamin D receptor, although this remains to be investigated.

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Basal and insulin stimulated glucose transport. Basal and insulin stimulated glucose transport in epididymal adipocytes from sham-treated rats (Control), rats treated with 1,25D3 [150 IU/Kg (3.75 μg/Kg) one a day, for 15 days] (1,25D3), streptozotocin-induced diabetic rats (STZ) and streptozotocin-induced diabetic rats treated with 1,25D3 (STZ+1,25D3). Values are the mean ± SEM of 6–7 determinations within each group. a p < 0.05 vs. Control-rats; b p < 0.05 vs. 1,25D3-rats; and c p < 0.05 vs. STZ-rats.
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Figure 3: Basal and insulin stimulated glucose transport. Basal and insulin stimulated glucose transport in epididymal adipocytes from sham-treated rats (Control), rats treated with 1,25D3 [150 IU/Kg (3.75 μg/Kg) one a day, for 15 days] (1,25D3), streptozotocin-induced diabetic rats (STZ) and streptozotocin-induced diabetic rats treated with 1,25D3 (STZ+1,25D3). Values are the mean ± SEM of 6–7 determinations within each group. a p < 0.05 vs. Control-rats; b p < 0.05 vs. 1,25D3-rats; and c p < 0.05 vs. STZ-rats.

Mentions: Treatment with 1,25D3 to non-diabetic rats did not alter basal or insulin-stimulated glucose transport in adipocytes from these animals (Figure 3). The injection of streptozotocin clearly decreased both basal and insulin-stimulated glucose transport. The treatment with 1,25D3 to streptozotocin-induced diabetic rats, improved by 107% the decreased basal glucose transport and by 71% the insulin-stimulated glucose transport in adipocytes from these diabetic animals (Figure 3).


Genomic actions of 1,25-dihydroxyvitamin D3 on insulin receptor gene expression, insulin receptor number and insulin activity in the kidney, liver and adipose tissue of streptozotocin-induced diabetic rats.

Calle C, Maestro B, García-Arencibia M - BMC Mol. Biol. (2008)

Basal and insulin stimulated glucose transport. Basal and insulin stimulated glucose transport in epididymal adipocytes from sham-treated rats (Control), rats treated with 1,25D3 [150 IU/Kg (3.75 μg/Kg) one a day, for 15 days] (1,25D3), streptozotocin-induced diabetic rats (STZ) and streptozotocin-induced diabetic rats treated with 1,25D3 (STZ+1,25D3). Values are the mean ± SEM of 6–7 determinations within each group. a p < 0.05 vs. Control-rats; b p < 0.05 vs. 1,25D3-rats; and c p < 0.05 vs. STZ-rats.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2533347&req=5

Figure 3: Basal and insulin stimulated glucose transport. Basal and insulin stimulated glucose transport in epididymal adipocytes from sham-treated rats (Control), rats treated with 1,25D3 [150 IU/Kg (3.75 μg/Kg) one a day, for 15 days] (1,25D3), streptozotocin-induced diabetic rats (STZ) and streptozotocin-induced diabetic rats treated with 1,25D3 (STZ+1,25D3). Values are the mean ± SEM of 6–7 determinations within each group. a p < 0.05 vs. Control-rats; b p < 0.05 vs. 1,25D3-rats; and c p < 0.05 vs. STZ-rats.
Mentions: Treatment with 1,25D3 to non-diabetic rats did not alter basal or insulin-stimulated glucose transport in adipocytes from these animals (Figure 3). The injection of streptozotocin clearly decreased both basal and insulin-stimulated glucose transport. The treatment with 1,25D3 to streptozotocin-induced diabetic rats, improved by 107% the decreased basal glucose transport and by 71% the insulin-stimulated glucose transport in adipocytes from these diabetic animals (Figure 3).

Bottom Line: These effects were accompanied by a normalization of the number of insulin receptors without altering receptor affinity but improving the insulin response to glucose transport in adipocytes from these diabetic animals.Moreover, a computer search in the rat insulin receptor promoter revealed the existence of two candidate vitamin D response element (VDRE) sequences located at -256/-219 bp and -653/-620 bp, the first overlapped by three and the second by four AP-2-like sites. these genomic actions of 1,25D3 could represent beneficial effects associated with the amelioration of diabetes via mechanisms that possibly involve direct transcriptional activation of the rat insulin receptor gene.The candidate VDREs identified may respond to 1,25D3 via activation of the vitamin D receptor, although this remains to be investigated.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, School of Medicine, Complutense University, 28040-Madrid, Spain. consuelo@med.ucm.es

ABSTRACT

Background: this study set out to examine the effects of the treatment with 1,25-dihydroxyvitamin D3 (1,25D3) [150 IU/Kg (3.75 microg/Kg) one a day, for 15 days] to non-diabetic rats and in rats rendered diabetic by a single injection of streptozotocin [65 mg/kg].

Results: treatment with 1,25D3 to non-diabetic rats did not affect the biochemical parameters measured in the plasma and urine of these animals. Likewise, insulin receptor expression in the kidney, liver, or adipose tissue and insulin-stimulated glucose transport in adipocytes from these animals were not affected either. Treatment with 1,25D3 to streptozotocin-induced diabetic rats did not correct the hyperglycemia, hypoinsulinemia, glycosuria or ketonemia induced by the diabetes, although it partially reversed the over-expression of the insulin receptor gene in the liver and adipose tissue, without altering the normal expression of this gene in the kidney. These effects were accompanied by a normalization of the number of insulin receptors without altering receptor affinity but improving the insulin response to glucose transport in adipocytes from these diabetic animals. Moreover, a computer search in the rat insulin receptor promoter revealed the existence of two candidate vitamin D response element (VDRE) sequences located at -256/-219 bp and -653/-620 bp, the first overlapped by three and the second by four AP-2-like sites.

Conclusion: these genomic actions of 1,25D3 could represent beneficial effects associated with the amelioration of diabetes via mechanisms that possibly involve direct transcriptional activation of the rat insulin receptor gene. The candidate VDREs identified may respond to 1,25D3 via activation of the vitamin D receptor, although this remains to be investigated.

Show MeSH
Related in: MedlinePlus