Correlation between nutrition intake and gene expression profiles in children with asthma

Pie, Jae Eun; Kim, Yu Ri; Kim, In Kyoung; Seo, Sungkyu; Lee, Seung Ho; Lee, Hee Ra; Yoo, Yung Joon; Chung, Ji Tae; Youn, Jong Pil; Oh, Moon Ju; Hwang, Seung Yong; Kim, Meyoung Kon

doi:10.1007/s13273-010-0042-1

Cited by 4 publications

(3 citation statements)

References 34 publications

(35 reference statements)

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“…Both ABCA1 and ABCG1 (related to cholesterol and phospholipid efflux) play a key role in severe pulmonary abnormalities such as asthma 27,28 . ABCA1-knockout mice exhibit massive lipid accumulation in alveolar macrophages, type II pneumocytes and lung parenchyma, abnormal lung morphology, and shallow breathing 27 .…”

Section: Discussionmentioning

confidence: 99%

Identification of genes induced by carbamazepine in human bronchial epithelial BEAS-2B cells

Song

Kim

Ryu

2011

Toxicol. Environ. Health Sci.

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Some drugs are limited in their clinical application due to their propensity for inducing adverse side effects. We examined some clinical chemotherapeutic agents that have pulmonary toxic effects. Carbamazepine (CBZ) is an antiepileptic agent and its long-term use is associated with interstitial pneumonia, pulmonary fibrosis, and pulmonary infiltration with eosinophilia. CBZ is persistent in the environment and is frequently detected in water systems. A new technique in toxicity screening, "toxicogenomic technology", represents a useful approach for evaluating the toxic properties of new drug candidates early in the drug discovery process and their potential effects on the environment. To this end, we have examined gene expression profiles in BEAS-2B cells (a human bronchial epithelial cell line) following exposure to CBZ, which induced pulmonary toxicity, by using a human oligonucleotide chip. We identified 518 up-and 496 down-regulated genes whose expression had changed by more than 1.5-fold ( p⁄0.01) following CBZ exposure. Gene Ontology (GO) analysis showed elevation in the expression of genes involved in several key biological processes related to pulmonary toxicity, such as cholesterol metabolism, cell proliferation, and cell cycle regulation. In conclusion, the present study indicates that CBZ exerts its toxicity by modulating mRNA expression in BEAS-2B cells. We suggest that genes expressed by CBZ might serve as a molecular signature, which could be used more widely when implemented in combination with more traditional techniques, for the assessment and prediction of toxicity following CBZ-exposure.

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Section: Discussionmentioning

confidence: 99%

Identification of genes induced by carbamazepine in human bronchial epithelial BEAS-2B cells

Song

Kim

Ryu

2011

Toxicol. Environ. Health Sci.

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“…The level of significance (fold change ≥ 1.3), while small, was considered significant as previous studies have shown that dietary intervention(s) tend to elicit somewhat modest, yet biologically meaningful, transcriptional responses [24,25]. The ID rats in each group exhibited modest, but significant alterations in the expression of genes representative of glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

Comparisons of the iron deficient metabolic response in rats fed either an AIN-76 or AIN-93 based diet

et al. 2012

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BackgroundPrevious studies examining the metabolic consequences of dietary iron deficiency have reported elevated serum glucose concentrations in iron-deficient animals. Importantly, the majority of these findings were observed using an earlier version of a laboratory animal diet (AIN-76A) in which the primary carbohydrate source was sucrose – a disaccharide known to negatively impact both glucose and lipid homeostasis. The AIN-76A diet formula was improved in 1993 (AIN-93) to optimize animal nutrition with a major change being the substitution of cornstarch for sucrose. Therefore, we sought to examine the effects of iron deficiency on steady-state glucose homeostasis and the hepatic expression of glucose- and lipid-related genes in rats fed an iron-deficient diet based on either an AIN-76A or AIN-93 diet.MethodsThe study design consisted of 6 treatment groups: control (C; 40 mg Fe/kg diet), iron deficient (ID; ≤ 3 mg Fe/kg diet), or pair-fed (PF; 40 mg Fe/kg) fed either an AIN-76A or AIN-93 diet for 21 d. Hemoglobin and hematocrit were measured in whole blood. Serum insulin and cortisol were measure by ELISA. Serum glucose and triacylglycerols were measured by standard colorimetric enzyme assays. Alterations in hepatic gene expression were determined by real-time qPCR.ResultsHemoglobin and hematocrit were significantly reduced in both ID groups compared to the C and PF groups. Similarly, animals in the both ID groups exhibited elevated steady-state levels of blood glucose and insulin, and significantly decreased levels of circulating cortisol compared to their respective PF controls. Serum triacyglycerols were only increased in ID animals consuming the AIN-76A diet. Hepatic gene expression analyses revealed a ~4- and 3-fold increase in the expression of glucokinase and pyruvate dehydrogenase kinase-4 mRNA, respectively, in the ID group on either diet compared to their respective PF counterparts. In contrast, the expression of lipogenic genes was significantly elevated in the AIN-76 ID group, while expression of these genes was unaffected by iron status in the AIN-93 ID group.ConclusionsThese results indicate that an impaired iron status is sufficient to alter glucose homeostasis, though alterations in lipid metabolism associated with ID are only observed in animals receiving the AIN-76A diet.

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“…Increased Gck expression has been shown increased on the glucose levels as a metabolic substrate, to increase glucose phosphorylation rate in the liver, responsible for blood glucose elevations. Furthermore, Gck may involve in the multiple pathways such as glycogen synthesis, glycolysis, and de novo lipogenesis which may explain the enhancing of the glucose utilization and hyperlipidemia in the responsible to dietary ID-animals [110][111][112][113][114][115][116]. In the studies of metabolic gene expression alterations indicate an impaired hepatic insulin response in ID-animals, exhibited as insulin resistance.…”

Section: Iron Deficiency and Diabetes Riskmentioning

confidence: 99%

Iron Homeostasis and Diabetes Risk

Tangvarasittichai

2018

CRDOJ

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Iron binds to protein in the form of heme and functions as co-factor of enzymes that mediate redox reactions for energy production and intermediate of metabolism. Individual iron status is reflected as the combination of nutritional and pathological diseases. Iron overload (IO) and iron deficiency anemia (IDA) are the risk factor for diabetes. The association of iron and diabetes was investigated in -thalassemia patients, in high dietary iron levels, and in iron deficiency anemia were also associated with diabetes risk. IO and IDA play the major role of oxidative stress and inflammation, mediated insulin resistance and -cell dysfunction to causal diabetes. The underlying mechanisms mediated of these effects still waiting for searching.

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Correlation between nutrition intake and gene expression profiles in children with asthma

Cited by 4 publications

References 34 publications

Identification of genes induced by carbamazepine in human bronchial epithelial BEAS-2B cells

Identification of genes induced by carbamazepine in human bronchial epithelial BEAS-2B cells

Comparisons of the iron deficient metabolic response in rats fed either an AIN-76 or AIN-93 based diet

Iron Homeostasis and Diabetes Risk

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