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

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.

Effect of Bis(maltolato)oxovanadium(IV) on Zinc, Copper, and Manganese Homeostasis and DMT1 mRNA Expression in Streptozotocin-Induced Hyperglycemic Rats

“…The levels of proinflammatory parameters, leptin, C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α) were determined in serum at day 35. These results are summarized in previous literature [ 14 ].…”

“…In identical working conditions, our research group described how treating rats with BMOV(IV) altered the homeostasis of Se [ 33 ], Mg [ 36 ] and Fe [ 34 ] and that these alterations were associated with changes in the antioxidant status. We also discovered that V treatment causes changes in serum levels of proinflammatory cytokines [ 14 ]. In the liver, we found that BMOV(IV) increased the activity of catalase (CAT), protein carbonyl groups and malonaldehyde (MDA) levels.…”

“…Methodology for glutathione peroxidase (GPx), glutathione reductase (GR); reduced glutathione (GSH), glutathione transferase (GST), superoxide dismutase (SOD), catalase (CAT), NAD(P)H: quinone-oxidoreductase-1 (NQO1), protein carbonyl group and malondialdehyde (MDA) determination have previously been described [ 33 , 34 ]. Moreover, at day 35, proinflammatory parameters (leptin, C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α)) were determined in serum following the methodology proposed by Sánchez-González et al [ 14 ].…”

“…Vanadium (V) is an essential element for some living organisms, but its role as a micronutrient has not yet been clarified. Moreover, some aspects of its role in cell metabolism, the toxicological implications and the therapeutic applications remain unknown [ 13 , 14 , 15 ]. Clarifying the metabolic implication of V in diabetes mellitus has received attention in recent years.…”

“…Nevertheless, some aspects of the V interaction with other metallic elements, especially antioxidant metals, remain unclear. The current use of V as an hypoglycemic agent is limited due to its pro-oxidant properties, cytokine production and inflammatory implications [ 14 , 20 ]. Several authors related the pro-oxidant activity of V to other trace elements, such as magnesium (Mg), iron (Fe), copper (Cu), selenium (Se) and/or zinc (Zn) [ 21 , 22 , 23 ].…”