• Journal of the Korea Society of Computer and Information
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• v.23 no.10
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• pp.135-141
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• 2018

In this paper, we propose to evaluate the effect of resistin-like molecule alpha ($Relm{\alpha}$) on the progression of anemia of inflammation. Anemia of inflammation is a common feature of inflammatory disorders, including chronic kidney disease, infections, and rheumatoid arthritis. $Relm{\alpha}$ is highly up-regulated in various inflammatory states, especially those involving asthma, intestinal inflammation, and parasitic diseases, and regulates the pathogenesis of those diseases. However, the role of $Relm{\alpha}$ in anemia of inflammation is unknown. To explore the roles of $Relm{\alpha}$ in anemia of inflammation in vivo, we generated mouse model of the disease by injecting 0.25 mg/kg lipopolysaccharides (LPS) intraperitoneally into $Relm{\alpha}-deficient$ and wild-type (WT) mice daily for 10 days. Research data was expressed as differences between LPS-treated $Relm{\alpha}-deficient$ and WT mice by a two-tailed non-parametric Mann-Whitney U-test using GraphPad Instat program. The results of the study are as follows: LPS-treated $Relm{\alpha}-deficient$ mice had significantly (p<0.05) lower hemoglobin contents, hematocrit levels and red blood cell indices including mean corpuscular volume, mean corpuscular hemoglobin than WT controls. This decrease was accompanied by significant (p<0.05) increase in total white blood cell and monocyte counts in the blood. However, there was no significant difference in mRNA levels of hepatic hepcidin and renal erythropoietin between the two animal groups. Taken together, these results indicates that $Relm{\alpha}$ deficiency exacerbates the anemia by increasing inflammation, suggesting therapeutic value of $Relm{\alpha}$ in the treatment of anemia of inflammation.

• Journal of Sport and Applied Science
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• v.6 no.4
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• pp.11-23
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• 2022

New insights into the aetiology of anaemia in athletes have been discovered in recent years. From hemodilution and redistribution, which are thought to commit to so-called "sports anaemia," to iron deficiency triggered by higher requirements, dietary requirements, decreased uptake, enhanced losses, hemolysis, and sequester, to genetic factors of different types of anaemia (some related to sport), anaemia in athletes necessitates a careful and multisystem methodology. Dietary factors that hinder iron absorption and enhance iron bioavailability (e.g., phytate, polyphenols) should be considered. Celiac disease, which is more common in female athletes, may be the consequence of an iron deficiency anaemia that is unidentified. Sweating, hematuria, gastrointestinal bleeding, inflammation, and intravascular and extravascular hemolysis are all ways iron is lost during strength training. In training, evaluating the iron status, particularly in athletes at risk of iron deficiency, may work on improving iron balance and possibly effectiveness. Iron status is influenced by a healthy gut microbiome. To eliminate hemolysis, athletes at risk of iron deficiency should engage in non-weight-bearing, low-intensity sporting activities.

• Environmental Mutagens and Carcinogens
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• v.25 no.4
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• pp.134-142
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• 2005

Liver cancer is a leading cause of tumor-related mortality, Diethylnitrosamine (DEN) is one of the most extensively studied hepatic carcinogens to date. In this study, the mRNA expression profile in DEN-induced liver tumors in mice was analyzed using DNA microarrays. We report increased expression of genes that participate in hypoxia response, including metallothionein 1 (Mt1), metallothionein 2 (Mt2), fatty acid synthase (Fasn), transferrin (Trf), adipose differentiation-related Protein (AdfP) and ceruloplasmin (CP), as well as those involved in predisposition and development of cancers, such as cytochrome P450 2A5 (Cyp2a5), alpha 2-HS-glycoprotein (Ahsg) and Jun-B oncogene (Junb). The hepatic iron regulatory peptide, hepcidin (Hampl), was downregulated in DEN-stimulated liver tumors. Expression of tumor suppressor genes, such as tripartite motif protein 13 (Trim13), was decreased under these conditions. The data collectively indicate that DEN-induced tumor development can be exploited as a possible model for liver cancer, since this process involves various genes with important functions in hepatic carcinogenesis.

• Psychiatry investigation
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• v.15 no.12
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• pp.1130-1134
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• 2018

Objective Trichotillomania is a relatively common illness whose neurobiology is poorly understood. One treatment for adult trichotillomania, n-acetyl cysteine (NAC), has antioxidative properties, as well as effects on central glutamatergic transmission. Preclinical models suggest that excessive oxidative stress may be involved in its pathophysiology. Methods Adults with trichotillomania provided a blood sample for analysis of compounds that may be influenced by oxidative stress [glutathione, angiotensin II, ferritin, iron, glucose, insulin and insulin growth factor 1 (IGF1), and hepcidin]. Participants were examined on symptom severity, disability, and impulsivity. The number of participants with out-of-reference range oxidative stress measures were compared against the null distribution. Correlations between oxidative stress markers and clinical measures were examined. Results Of 14 participants (mean age 31.2 years; 92.9% female), 35.7% (n=5) had total glutathione levels below the reference range (p=0.041). Other oxidative stress measures did not have significant proportions outside the reference ranges. Lower levels of glutathione correlated significantly with higher motor impulsiveness (Barratt Impulsiveness Scale sub-score) (r=0.97, p=0.001). Conclusion A third of patients with trichotillomania had low levels of glutathione, and lower levels of glutathione correlated significantly with higher motor impulsiveness. Because NAC is a precursor for cysteine, and cysteine is a rate limiting step for glutathione production, these results may shed light on the mechanisms through which NAC can have beneficial effects for impulsive symptoms. Confirmation of these results requires a suitable larger follow-up study, including an internal normative control group.

• Clinical Nutrition Research
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• v.11 no.4
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• pp.316-330
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• 2022

Iron plays a role in energy metabolism as a component of vital enzymes and electron transport chains (ETCs) for adenosine triphosphate (ATP) synthesis. The tricarboxylic acid (TCA) cycle and oxidative phosphorylation are crucial in generating ATP in mitochondria. At the mitochondria matrix, heme and iron-sulfur clusters are synthesized. Iron-sulfur cluster is a part of the aconitase in the TCA cycle and a functional or structural component of electron transfer proteins. Heme is the prosthetic group for cytochrome c, a principal component of the respiratory ETC. Regarding fat metabolism, iron regulates mitochondrial fat oxidation and affects the thermogenesis of brown adipose tissue (BAT). Thermogenesis is a process that increases energy expenditure, and BAT is a tissue that generates heat via mitochondrial fuel oxidation. Iron deficiency may impair mitochondrial fuel oxidation by inhibiting iron-containing molecules, leading to decreased energy expenditure. Although it is expected that impaired mitochondrial fuel oxidation may be restored by iron supplementation, its underlying mechanisms have not been clearly identified. Therefore, this review summarizes the current evidence on how iron regulates energy metabolism considering the TCA cycle, oxidative phosphorylation, and thermogenesis. Additionally, we relate iron-mediated metabolic regulation to obesity and obesity-related complications.