Vanadium Decreases Hepcidin mRNA Gene Expression in STZ-Induced Diabetic Rats, Improving the Anemic State.

Cristina Sánchez-González,Francesca Algieri,María Montes-Bayón,Julio Gálvez,Alba Rodríguez-Nogales,Pilar Aranda,Juan Llopis,Lorenzo Rivas-García

doi:10.3390/nu13041256

Cristina Sánchez-González, Francesca Algieri + Show 6 more

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https://doi.org/10.3390/nu13041256

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Abstract

Diabetes is a disease with an inflammatory component that courses with an anemic state. Vanadium (V) is an antidiabetic agent that acts by stimulating insulin signaling. Hepcidin blocks the intestinal absorption of iron and the release of iron from its deposits. We aim to investigate the effect of V on hepcidin mRNA expression and its consequences on the hematological parameters in streptozotocin-induced diabetic Wistar rats. Control healthy rats, diabetic rats, and diabetic rats treated with 1 mgV/day were examined for five weeks. The mineral levels were measured in diet and serum samples. Hepcidin expression was quantified in liver samples. Inflammatory and hematological parameters were determined in serum or whole blood samples. The inflammatory status was higher in diabetic than in control rats, whereas the hematological parameters were lower in the diabetic rats than in the control rats. Hepcidin mRNA expression was significantly lower in the V-treated diabetic rats than in control and untreated diabetic rats. The inflammatory status remained at a similar level as the untreated diabetic group. However, the hematological profile improved after the V-treatment, reaching similar levels to those found in the control group. Serum iron level was higher in V-treated than in untreated diabetic rats. We conclude that V reduces gene expression of hepcidin in diabetic rats, improving the anemic state caused by diabetes.

Highlights

Vanadium (V) is widely distributed and essential for some living organisms, but its role as a micronutrient for humans, its essentiality, distribution, toxicology, and biological and pharmacological activities are still not fully understood
The present study aimed to examine whether the treatment of diabetic rats with V causes hematological changes and whether such changes are related to changes in hepcidin expression and the secretion of pro-inflammatory factors, previously demonstrated in healthy rats [22,23]
Some gastrointestinal disorders were found in two animals for the group of rats treated with V; these animals were removed from the study

Summary

Introduction

Vanadium (V) is widely distributed and essential for some living organisms, but its role as a micronutrient for humans, its essentiality, distribution, toxicology, and biological and pharmacological activities are still not fully understood. Clinical trials for some V compounds have been completed, many aspects remain to be studied, such as their interactions with other elements involved in homeostasis. A growing interest in the pharmacological effects, such as hypoglycemic or insulin-mimetic properties [1,2,3,4], has led V metabolism to become an important area of current research. The insulin-mimetic activity of V and its possible application as a hypoglycemic agent is associated with the combination of these three effects [1,2,3,4,5]. Some interaction between other trace elements could reduce the toxicity associated with V [7]

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