Cross-Talk Between Body Iron Stores and Diabetes: Iron Stores are Associated with Activity and Microsatellite Polymorphism of the Heme Oxygenase and Type 2 Diabetes

Arredondo, Miguel; Fuentes, Marcela; Jorquera, Denisse; Candia, Valeria; Carrasco, Elena; Leiva, Elba; Mujica, Verónica; Hertrampf, Eva; Pérez, Francisco

doi:10.1007/s12011-010-8895-7

Cited by 20 publications

(14 citation statements)

References 24 publications

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“…However, increasing iron store is not necessarily a usual factor for diabetes. Their results supported the idea that patients with increased iron stores have a higher predisposition to develop noninsulin-dependent diabetes (29).…”

Section: Discussionsupporting

confidence: 63%

Effect of treatment of iron deficiency anemia onhemoglobin A1c in type 2 diabetic patients

Nasli‐Esfahani¹,

Larijani²,

Amini³

et al. 2017

Turk J Med Sci

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Background/aim: Iron deficiency anemia (IDA) affects hemoglobin A1c (HbA1c) levels. This study aimed to evaluate the effect of treatment of iron deficiency anemia on hemoglobin A1c in type 2 diabetic patients. Materials and methods:Ninety type 2 diabetes mellitus (T2DM) patients with IDA were included in a randomized, placebo-controlled, single-blind clinical trial. The intervention group (n = 45) received 200 mg/day oral iron for 3 months and the control group (n = 45) received an oral placebo for the same period. Fasting blood sugar, complete blood count, and HbA1c were measured for all subjects at the beginning and the end of the trial. Results:The mean age of the treatment and control group was 51.47 ± 1.05 and 52 ± 1.1 years, respectively. The two groups were not statistically significantly different with regard to diabetes duration (P = 0.436) and age (P = 0.617). Hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin, serum iron, ferritin, total iron-binding capacity, and HbA1c were significantly improved in the intervention group in comparison with the control group (P = 0.005). Conclusion:Iron status should be considered during the interpretation of the HbA1c concentrations in diabetes mellitus. Iron replacement therapy can decrease HbA1c in anemic patients with IDA and T2DM.

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Section: Discussionsupporting

confidence: 63%

Effect of treatment of iron deficiency anemia onhemoglobin A1c in type 2 diabetic patients

Nasli‐Esfahani¹,

Larijani²,

Amini³

et al. 2017

Turk J Med Sci

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“…2012 was excluded from the sTfR meta‐analysis as investigated particiants likely overlap with the study by Arredondo et al . 2011 .…”

Section: Resultsmentioning

confidence: 99%

Association of iron indices and type 2 diabetes: a meta‐analysis of observational studies

Orban

Schwab

Thorand

et al. 2014

Diabetes Metabolism Res

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The literature on the role of body iron status in the development of type 2 diabetes (T2D) in humans is inconsistent. We aimed to assess the association between iron indices and T2D by a meta-analysis of previously published studies. A systematic literature search was conducted in PubMed and EMBASE. Observational studies on the association of ferritin (when controlled for age and sex), transferrin saturation, soluble transferrin receptor and transferrin with T2D were included. Pooled association estimates were calculated using a random effects model. Forty-six eligible studies were identified. The pooled multivariable adjusted relative risks of T2D in the highest versus lowest quartile of ferritin levels were significantly elevated in both cross-sectional as well as prospective studies and after restriction to inflammation-adjusted studies [overall: 1.67 (95% CI 1.41-1.99)]. The mean difference indicated 43.54 ng/mL (95% CI 28.14-58.94) higher ferritin levels in type 2 diabetic individuals. The relative risk for a transferrin saturation ≥ 50% was 1.59 (95% CI 1.28-1.97), the mean difference was -1.92% [95% CI -2.99-(-0.85)]. Study-specific results of soluble transferrin receptor and transferrin levels were extremely heterogeneous. Ferritin and clinically elevated transferrin saturation were strongly associated with an increased risk of T2D, overall and in prospective studies. Ferritin was also significantly associated after multivariable adjustment including inflammation. Thus, the current evidence hints at a causal effect; however, publication bias and unmeasured confounding cannot be excluded.

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“…Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron-deficiency anemia (with paradoxical increased levels of ferritin) [7] . Determining the role that HO-1 plays in such regulatory mechanisms has become increasingly relevant in recent years because its induction has been shown to prevent ethanol-induced inflammation in the intestine [36] and liver [4] , as well as in the prevention of oxidative damage to hepatocytes [5] .…”

Section: The Physiological Role Of the Ho-1 Gene In The Livermentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of REVIEW 541October 27, 2013|Volume 5|Issue 10| WJH|www.wjgnet.com low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

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Cross-Talk Between Body Iron Stores and Diabetes: Iron Stores are Associated with Activity and Microsatellite Polymorphism of the Heme Oxygenase and Type 2 Diabetes

Cited by 20 publications

References 24 publications

Effect of treatment of iron deficiency anemia onhemoglobin A1c in type 2 diabetic patients

Effect of treatment of iron deficiency anemia onhemoglobin A1c in type 2 diabetic patients

Association of iron indices and type 2 diabetes: a meta‐analysis of observational studies

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

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