Plasma iron status in elite weightlifters after four weeks of intensive training

2019 ◽  
Vol 34 (5) ◽  
pp. 328.e1-328.e8
Author(s):  
R. Khlif ◽  
R. Marrakchi ◽  
K. Jamoussi ◽  
Z. Sahnoun ◽  
H. Chtourou ◽  
...  
Keyword(s):  
Iron Status ◽  
Intensive Training ◽  
Plasma Iron

Effect of iron status on DMT1 expression in duodenal enterocytes from β2-microglobulin knockout mice

2002 ◽  
Vol 283 (3) ◽  
pp. G687-G694 ◽  
Author(s):  
Torben Moos ◽  
Debbie Trinder ◽  
Evan H. Morgan
Keyword(s):  
Iron Status ◽  
Apical Cell ◽  
Genetic Defect ◽  
Iron Concentration ◽  
Iron Availability ◽  
Western Blots ◽  
Dietary Regimen ◽  
Apical Cell Membrane ◽  
Plasma Iron ◽  
Poor Diet

Divalent metal transporter I (DMT1) is thought to be involved in transport of iron across the apical cell membrane of villus duodenal cells. To determine its role in hereditary hemochromatosis (HH), we used β2-microglobulin knockout ( B2M−/−) mice that accumulate iron as in HH. The B2M−/− and control C57BL/6 ( B2M+/+) mice were fed diets with different iron contents. Increasing the iron availability increased plasma iron levels in both B2M+/+ and B2M−/−mice. Reducing the iron availability decreased the plasma iron concentration in B2M+/+ mice but was without effect on plasma iron in B2M−/− mice. DMT1 was not detectable in mice fed normal or iron-loaded diets when using immunohistochemistry. In Western blots, however, the protein was consistently observed regardless of the dietary regimen. DMT1 expression was increased to the same extent in B2M+/+ and B2M−/− mice when fed an iron-poor diet. In both strains of mice fed an iron-poor diet, DMT1 was evenly distributed in the differentiated enterocytes from the base to the tip of the villi but was absent from the crypts of Lieberkühn. These data suggest that the observed effects were due to the state of iron deficiency in mucosal cells rather than genetic defect.

scholarly journals Common variants in the transmembrane protease serine 6 (TMPRSS6) gene alter hepcidin but not plasma iron in response to oral iron in healthy Gambian adults: a recall-by-genotype study

2021 ◽  
Author(s):  
Momodou W Jallow ◽  
Susana Campino ◽  
Alasana Saidykhan ◽  
Andrew M Prentice ◽  
Carla Cerami
Keyword(s):  
Oral Dose ◽  
Iron Status ◽  
Association Studies ◽  
Oral Iron ◽  
Genome Wide Association Studies ◽  
Genetic Determinants ◽  
Plasma Iron ◽  
Risk Alleles ◽  
Genome Wide ◽  
Iron Parameters

Abstract Background The role of genetic determinants in mediating iron status in Africans is not fully understood. Genome-wide association studies in non-African populations have revealed genetic variants in the TMPRSS6 gene that are associated with the risk of anemia. Objectives To investigated the effects of risk alleles for low iron status from TMPRSS6 rs2235321, rs855791 and rs4820268, on responses to oral iron in healthy Gambian adults. Methods Using a recall-by-genotype design, participants were selected from a pre-genotype cohort of 3000 individuals in the Keneba Biobank (MRCG at LSHTM). Participants were invited to participate in the study based on nine genotype combinations obtained from three TMPRSS6 SNPs (rs2235321, rs855791 and rs4820268). The participants fasted overnight and then ingested a single oral dose of ferrous sulfate (130 mg elemental iron). Blood samples were collected prior to iron ingestion and at 2 and 5 hours after the oral iron dose. The effects of genotype on hepcidin and plasma iron parameters were assessed. Results A total of 251 individuals were enrolled. Homozygous carriers of the major TMPRSS6 alleles at each of the SNPs had higher plasma hepcidin at baseline (rs2235321: GG vs AA 9.50 vs 6.60ng/ml,  p = 0.035; rs855791: GG vs AG = 9.50 vs 4.96ng/mL,  p = 0.015; rs4820268: AA vs GG = 9.50 vs 3.27ng/mL,  p = 0.002) and at subsequent timepoints. There were no differences in delta plasma iron (a proxy for iron absorption) between genotypes. In most subjects, hepcidin levels increased following iron ingestion (overall group mean = 4.98 ± 0.98ng/ml at 5h,  p < 0.001),  but double heterozygotes at rs2235321 and rs855791 showed no increase (0.36 ± 0.40ng/ml at 5h,  p = 0.667). Conclusions This study revealed that common TMPRSS6 variants influence hepcidin concentrations, but not iron status indicators either at baseline or following a large oral dose of iron. These results suggest that genetic variations in the TMPRSS6 gene are unlikely to be important contributors to variations in iron status in Africans. This study was registered at ClinicalTrials.gov # NCT03341338.

Non Transferrin Bound Labile Plasma Iron and Iron Overload in Sickle Cell Disease: a Comparative Study Between Sickle Cell Disease and β Thalassemic Patients.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4625-4625
Author(s):  
Ariel Koren ◽  
Daniel Fink ◽  
Osnat Admoni ◽  
Yardena Tennenbaum-Rakover ◽  
Carina Levin
Keyword(s):  
Sickle Cell Disease ◽  
Iron Overload ◽  
Sickle Cell ◽  
Research Funding ◽  
Iron Status ◽  
Blood Transfusions ◽  
Grey Zone ◽  
Cell Disease ◽  
Plasma Iron ◽  
Oncology Research

Abstract Abstract 4625 BACKGROUND Blood transfusions are the standard of care in β thalassemia and transfusions are also indicated in Sickle Cell Disease (SCD) patients with hypersplenism, recurrent vaso-occlusive crises and for stroke prevention. Iron overload caused by blood transfusions in thalassemia and in SCD may affect morbidity and mortality. Recent studies of iron overload in SCD suggest that the biologic features of SCD and the chronic inflammatory state may protect SCD patients from iron damage. DESIGNS AND METHODS In view of the controversy regarding the effect of iron overload in patients with SCD we studied the iron status, including non transferrin bound iron (NTBI) and labile plasma iron (LPI) levels in a cohort of thirty six SCD patients and compare the results with 43 thalassemia patients. RESULTS Our results indicate that none of the SCD patients had clinical symptoms of iron overload. Only two SCD patients had NTBI values in the grey zone (0.4 units) and none had positive values. By contrast, 14 patients with Thalassemia Major and 3 with Thalassemia Intermedia had NTBI values above 0.6, level that are in the positive pathological range. Similarly, four thalassemia patients, but only one SCD patient had positive LPI levels. CONCLUSIONS The parameters of iron status in SCD patients, even after frequent transfusions are different when compared to patients with thalassemia. The low NTBI and LPI levels found in patients with SCD are in keeping with the absence of clinical signs of iron overload in this disease. Disclosures: Koren: Novartis Oncology: Research Funding. Levin:Novartis Oncology: Research Funding.

scholarly journals Low plasma iron status and akathisia.

1990 ◽  
Vol 53 (8) ◽  
pp. 671-674 ◽  
Author(s):  
A Barton ◽  
J Bowie ◽  
K Ebmeier
Keyword(s):  
Iron Status ◽  
Plasma Iron

scholarly journals Low plasma iron status and akathisia.

1991 ◽  
Vol 54 (9) ◽  
pp. 847-847 ◽  
Author(s):  
T Tarao ◽  
R Yoshimura
Keyword(s):  
Iron Status ◽  
Plasma Iron

Supplementation with beta-hydroxy-beta-methylbutyrate impacts glucose homeostasis and increases liver size in trained mice

2020 ◽  
Vol 90 (1-2) ◽  
pp. 113-123
Author(s):  
Ines Schadock ◽  
Barbara G. Freitas ◽  
Irae L. Moreira ◽  
Joao A. Rincon ◽  
Marcio Nunes Correa ◽  
...  
Keyword(s):  
Strength Training ◽  
Muscle Mass ◽  
Glucose Homeostasis ◽  
Fasting Blood Glucose ◽  
Hepatic Metabolism ◽  
Mass Gain ◽  
Trained Group ◽  
Tissue Mass ◽  
Liver Size ◽  
Intensive Training

Abstract. β-hydroxy-β-methyl butyrate (HMB) is a bioactive metabolite derived from the amino acid leucine, usually applied for muscle mass increase during physical training, as well as for muscle mass maintenance in debilitating chronic diseases. The hypothesis of the present study is that HMB is a safe supplement for muscle mass gain by strength training. Based on this, the objective was to measure changes in body composition, glucose homeostasis and hepatic metabolism of HMB supplemented mice during strength training. Two of four groups of male mice (n = 6/group) underwent an 8-week training period session (climbing stairs) with or without HMB supplementation (190 mg/kgBW per day). We observed lower body mass gain (4.9 ± 0.43% versus 1.2 ± 0.43, p < 0.001) and increased liver mass (40.9 ± 0.9 mg/gBW versus 44.8 ± 1.3, p < 0.001) in the supplemented trained group compared with the non-supplemented groups. The supplemented trained group had an increase in relative adipose tissue mass (12.4 ± 0.63 mg/gBW versus 16.1 ± 0.88, P < 0.01) compared to the non-supplemented untrained group, and an increase in fasting blood glucose (111 ± 4.58 mg/dL versus 122 ± 3.70, P < 0.05) and insulin resistance (3.79 ± 0.19 % glucose decay/min versus 2.45 ± 0.28, P < 0.05) comparing with non-supplemented trained group. Adaptive heart hypertrophy was observed only in the non-supplemented trained group (4.82 ± 0.05 mg/gBW versus 5.12 ± 0.13, P < 0.05). There was a higher hepatic insulin-like growth factor-1 expression (P = 0.002) in supplemented untrained comparing with non-supplemented untrained group. Gene expression of gluconeogenesis regulatory factors was increased by training and reduced by HMB supplementation. These results confirm that HMB supplementation associated with intensive training protocol drives changes in glucose homeostasis and liver metabolism in mice.

Iron status in diabetes mellitus

2019 ◽  
pp. 7-12
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Defense Mechanism ◽  
Acute Stress ◽  
Islet Cells ◽  
Iron Status ◽  
Acute Phase Reactant ◽  
Iron Deposition ◽  
Muscle Tissues ◽  
High Production

Diabetes mellitus can be defined as chronic metabolic disease which results from either relative or complete absence of insulin by the pancreatic beta islet cells. This in-turn may lead to hyperglycemia due to disturbances in the metabolism of glucose. In the human body, iron is con- sidered to be an effective pro-oxidant and participates in the generation of reactive oxygen species (ROS) such as hydroxyl radical. Because of the poor antioxidant defense mechanism of beta cells (low production of antioxidant enzymes such as catalase, glutathione peroxidase and dismutase), so they are highly prone to iron-induced oxidative stress and iron deposition in it and this will lead to apoptosis, and subsequently insulin deficiency. This iron deposition in beta cells will also lead to insulin resistance by reducing insulin extracting ability of the liver and inhibiting glucose uptake in muscle tissues and fats, this in turn will result in high production of hepatic glucose. Ferritin which is an acute phase reactant protein, that responds to acute stress like trauma, infections, tissue necrosis and surgery, it can produce diabetes mellitus either through inflammation or by increasing iron stores.

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