Psychological stress induces hypoferremia through the IL-6–hepcidin axis in rats

Zhao, Min; Chen, Jianbo; Wang, Wanyin; Wang, Lei; Ma, Long; Shen, Hui; Li, Min

doi:10.1016/j.bbrc.2008.05.166

Cited by 38 publications

(39 citation statements)

References 28 publications

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“…IL-6 is an inXammatory signal which induces the synthesis of the iron regulatory hormone hepcidin (Nemeth et al 2003, resulting in hypoferremia ) and increased iron storage within the reticuloendothelial system (Nicolas et al 2002). It should also be noticed that, besides increased muscular workload, psychological stress induces expression of IL-6 and therefore should be taken into account when interpreting hepcidin data (Goebel et al 2000;Zhao et al 2008). However, as previously mentioned, most clinical data on the impact of exercise and iron changes have so far concerned intense muscle activity with eccentric contractions as marathon running, in which muscle damage, inXammatory response and increased iron needs for myoglobin synthesis were expected (Ahmadi et al 2008).…”

Section: Discussionmentioning

confidence: 96%

Daily regulation of serum and urinary hepcidin is not influenced by submaximal cycling exercise in humans with normal iron metabolism

et al. 2009

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Hepcidin and hemojuvelin (HJV) are two critical regulators of iron metabolism as indicated by the development of major iron overload associated to mutations in hepcidin and HJV genes. Hepcidin and HJV are highly expressed in liver and muscles, respectively. Intensive muscular exercise has been reported to modify serum iron parameters and to increase hepcidinuria. The present study aimed at evaluating the potential impact of low intensity muscle exercise on iron metabolism and on hepcidin, its key regulator. Fourteen normal volunteers underwent submaximal cycling-based exercise in a crossover design and various iron parameters, including serum and urinary hepcidin, were serially studied. The results demonstrated that submaximal ergocycle endurance exercise did not modulate hepcidin. This study also indicated that hepcidinuria did not show any daily variation whereas serum hepcidin did. The findings, by demonstrating that hepcidin concentrations are not influenced by submaximal cycling exercise, may have implications for hepcidin sampling in medical practice.

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Section: Discussionmentioning

confidence: 96%

Daily regulation of serum and urinary hepcidin is not influenced by submaximal cycling exercise in humans with normal iron metabolism

et al. 2009

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“…We found in our previous study that stress could cause iron metabolism disruption in some organs in rats, and iron deposition in the hippocampus was significantly higher than those in other cerebral regions after psychological stress (PS) exposure [3][4][5][6]. Studies have also found that long-term depression could lead to decreased hippocampus volume and neuron death in the hippocampus [7].…”

Section: Dmt1 Divalent Metal Transporter 1 Irementioning

confidence: 80%

Corticosterone Induces Dysregulation of Iron Metabolism in Hippocampal Neurons In Vitro

Wang

et al. 2009

Biol Trace Elem Res

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Iron is required for neuronal function but in excess generates neurodegeneration. Although the iron homeostasis machinery in neurons has been described extensively, little is known about the influence of corticosterone on the iron homeostasis in neurons. In this study, we characterized the response of hippocampal neurons to a model of progressive corticosterone condition. We found that increasing extracellular corticosterone-induced iron accumulation killed a large proportion of neurons. Iron concentrations were significantly increased in the corticosterone-treated cells. In the hippocampal neurons, corticosterone decreased expression of ferritin and increased expression of transferrin receptor1 (TfR1), iron regulatory protein1 (IRP1), and divalent metal transporter 1. Corticosterone-induced elevation of IRP1 expression can cause increase of TfR1 and decrease of ferritin expression, which further leads to iron accumulation in hippocampal neurons and subsequently increases the oxidative damage of the neurons; it is indicated that corticosterone might be an important reason for iron deposition-caused neurodegenerative diseases.

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“…Induction of hypoferremia through the IL-6-hepcidin axis has been shown in 3-day and 7-day exposure to repeated psychosocial stress in rats using the communication box paradigm [12][13][14]. The observed changes reversed after injecting anti-IL-6 antibody, establishing the causality.…”

Section: Introductionmentioning

confidence: 84%

Adolescent Life-Event Stress in Boys Is Associated with Elevated IL-6 and Hepcidin but Not Hypoferremia

Augustine

Nair

Rao

et al. 2014

Journal of the American College of Nutrition

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Psychological stress induces hypoferremia through the IL-6–hepcidin axis in rats

Cited by 38 publications

References 28 publications

Daily regulation of serum and urinary hepcidin is not influenced by submaximal cycling exercise in humans with normal iron metabolism

Daily regulation of serum and urinary hepcidin is not influenced by submaximal cycling exercise in humans with normal iron metabolism

Corticosterone Induces Dysregulation of Iron Metabolism in Hippocampal Neurons In Vitro

Adolescent Life-Event Stress in Boys Is Associated with Elevated IL-6 and Hepcidin but Not Hypoferremia

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