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      The Combined Effects of Iron Excess in the Diet and Chromium(III) Supplementation on the Iron and Chromium Status in Female Rats

      research-article
      1 , , 2
      Biological Trace Element Research
      Springer US
      Chromium(III) propionate complex, Fe excess, Iron, Chromium, Rats

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          Abstract

          Inadequate iron supply has significant consequences to health. There are some relations between the metabolism of different trace elements, such as iron, zinc, copper and chromium. However, the direction of these interactions can be antagonistic or synergistic, and it depends on many factors. The aim of the study was to evaluate the combined effects of supplementary of chromium(III) propionate complex (Cr3) with iron excess on the Cr and Fe status in healthy female rats. The 36 healthy female Wistar rats were divided into six experimental groups (six animals in each) with different Fe levels—adequate (45 mg kg −1—100% RDA) and high (excessive—180 mg kg −1—400% RDA). At the same time, they were supplemented with Cr(III) at doses of 1, 50 and 500 mg kg −1 of diet: C1—control (Fe 45 mg kg −1, Cr 1 mg kg −1); C50 (Fe 45 mg kg −1, Cr 50 mg kg −1); C500 (Fe 45 mg kg −1, Cr 500 mg kg −1); H1 (Fe 180 mg kg −1, Cr 1 mg kg −1); H50 (Fe 180 mg kg −1, Cr 50 mg kg −1); H500 (Fe 180 mg kg −1, Cr 500 mg kg −1). The serum iron level and total iron binding capacity (TIBC) were measured with colorimetric methods. The serum ferritin level was measured by means of electrochemiluminescence immunoassay. The serum transferrin level was measured with the ELISA method. Haematological measurements were made with an automated blood analyser. The Cr and Fe tissular levels were measured with the AAS method. The exposure to a high level of Fe(III) alone or in combination with Cr caused Fe accumulation in tissues, especially in the liver and kidneys, but there were no significant changes in the TIBC, transferrin, ferritin concentration in the serum and most haematological parameters. Moreover, the serum, hepatic and renal Cr concentrations decreased. The doses of supplementary Cr(III) given separately or in combination with high level of Fe(III) disturbed the Cr content in the liver and kidneys of healthy female rats. However, they did not change most of the parameters of Fe metabolism, except the Fe kidney concentration. Supplementary Cr3 decreased the renal Fe level in groups with adequate Fe content in the diet. However, the renal Fe levels increased along with a higher Cr level in the diet in groups with high Fe content. The findings proved a relationship between Fe(III) and Cr(III) metabolism in healthy female rats. However, the direction of change varied and depended on relative amounts of these elements in the diet.

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          Iron and diabetes risk.

          Iron overload is a risk factor for diabetes. The link between iron and diabetes was first recognized in pathologic conditions-hereditary hemochromatosis and thalassemia-but high levels of dietary iron also impart diabetes risk. Iron plays a direct and causal role in diabetes pathogenesis mediated both by β cell failure and insulin resistance. Iron also regulates metabolism in most tissues involved in fuel homeostasis, with the adipocyte in particular serving an iron-sensing role. The underlying molecular mechanisms mediating these effects are numerous and incompletely understood but include oxidant stress and modulation of adipokines and intracellular signal transduction pathways. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Components of the AIN-93 diets as improvements in the AIN-76A diet.

            P G Reeves (1997)
            The AIN-93 rodent diets were formulated to substitute for the previous version (AIN-76A) and to improve the performance of animals that consume them. They are called AIN-93G, formulated for growth, and AIN-93M, for maintenance. Major changes included substituting cornstarch for sucrose and soybean oil for corn oil and increasing the amount in order to supply both essential fatty acids (linoleic and linolenic). L-Cystine was substituted for DL-methionine to supplement the casein component. The mineral mix was reformulated to lower the amounts of phosphorus, manganese and chromium, to increase the amount of selenium, and to add molybdenum, silicon, fluoride, nickel, boron, lithium and vanadium. The amounts of vitamins E, K-1 and B-12 were increased over those in the AIN-76A vitamin mix. The AIN-93G diet contains 200 g of casein and 70 g of soybean oil/kg diet. The maintenance diet (AIN-93M) contains 140 g of casein and 40 g of soybean oil/kg diet. The 1993 diets have a better balance of essential nutrients than the 1976 diet and are better choices for studies with laboratory rodents.
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              Oxidative stress, beta-cell apoptosis, and decreased insulin secretory capacity in mouse models of hemochromatosis.

              The pathogenesis of diabetes associated with hemochromatosis is not known. We therefore examined glucose homeostasis and beta-cell function in mouse models of hemochromatosis. Mice with targeted deletion of the hemochromatosis gene (Hfe(-/-)) on the 129/Sv genetic background exhibited a 72% increase in iron content in the islets of Langerhans compared with wild-type controls. Insulin content was decreased in Hfe(-/-) mice by 35%/pancreas and 25%/islet. Comparable decreases were seen in the mRNA levels of beta-cell-specific markers, ins1, ins2, and glucose transporter 2. By 6-8 months, islets from Hfe(-/-) mice were 45% smaller, associated with increased staining for activated caspase 3 and terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick end labeling. Islets from Hfe(-/-) mice were also desensitized to glucose, with half-maximal stimulation of insulin secretion seen at 16.7 +/- 0.9 mm glucose in perifused islets from Hfe(-/-) mice compared with 13.1 +/- 0.6 mm glucose in wild-type animals. Carbonyl protein modification, a marker for oxidative stress, was increased by 58% in Hfe(-/-) islets. Despite decreased islet size, Hfe(-/-) mice exhibited enhanced glucose tolerance. Fasting serum insulin levels were comparable between Hfe(-/-) and Hfe(+/+) mice, but were 48% lower in the Hfe(-/-) mice 30 min after challenge. Similar results were seen in mice carrying an Hfe mutation analogous to the common human mutation (C282Y) and in mice fed excess dietary iron. Hfe(-/-)mice on the C57BL6 background exhibited decreased glucose tolerance at 10-12 months due to an inability to increase insulin levels as they aged. We conclude that iron excess results in beta-cell oxidant stress and decreased insulin secretory capacity secondary to beta-cell apoptosis and desensitization of glucose-induced insulin secretion. This abnormality alone, however, is insufficient to cause diabetes.
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                Author and article information

                Contributors
                halina.staniek@up.poznan.pl
                Journal
                Biol Trace Elem Res
                Biol Trace Elem Res
                Biological Trace Element Research
                Springer US (New York )
                0163-4984
                1559-0720
                21 November 2017
                21 November 2017
                2018
                : 184
                : 2
                : 398-408
                Affiliations
                [1 ]ISNI 0000 0001 2157 4669, GRID grid.410688.3, Institute of Human Nutrition and Dietetics, Department of Bromatology and Food Toxicology, , Poznań University of Life Sciences, ; ul. Wojska Polskiego 31, 60-624 Poznań, Poland
                [2 ]ISNI 0000 0001 2205 0971, GRID grid.22254.33, Department of Clinical Psychology, , Poznań University of Medical Sciences, ; ul. Bukowska 70, 60-812 Poznań, Poland
                Author information
                http://orcid.org/0000-0001-8597-1057
                Article
                1203
                10.1007/s12011-017-1203-z
                6061187
                29164513
                75469113-e45c-49b6-b9d1-10c005deb0b9
                © The Author(s) 2017

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 21 September 2017
                : 13 November 2017
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100005857, Uniwersytet Przyrodniczy w Poznaniu;
                Award ID: 507.786.29 and 507.786.44
                Award Recipient :
                Categories
                Article
                Custom metadata
                © Springer Science+Business Media New York 2018

                Biochemistry
                chromium(iii) propionate complex,fe excess,iron,chromium,rats
                Biochemistry
                chromium(iii) propionate complex, fe excess, iron, chromium, rats

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