Hypoferræmia in Obese Adolescents

Wenzel, Barbara; Stults, HarryB.; Mayer, Jean

doi:10.1016/s0140-6736(62)90110-1

Cited by 208 publications

(96 citation statements)

References 8 publications

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“…In our children, all three inflammatory markers (CRP, IL-6 and leptin) significantly increased with increasing adiposity, and CRP was a significant predictor of SF, but not TfR, independent of adiposity. Thus, our data indicate poorer iron status in overweight compared with normal weight children, consistent with previous studies 1,[4][5][6]9 and emphasize the limitations of SF as an iron status indicator in overweight individuals. It has been suggested that obesity may be associated with a low-quality diet containing little iron.…”

Section: Discussionsupporting

confidence: 92%

Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children

2009

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Background: Obesity increases the risk for iron deficiency, but the underlying mechanism is unclear. It is possible that overweight individuals may have lower dietary iron intake and/or bioavailability. Alternatively, obesity-related inflammation may increase hepcidin concentrations and reduce iron availability. Circulating hepcidin levels have not been compared in normal weight vs overweight individuals. Objective: The objective of this study was to compare iron status, dietary iron intake and bioavailability, as well as circulating levels of hepcidin, leptin and interleukin-6 (IL-6), in overweight vs normal weight children. Design: In 6-14-year-old normal and overweight children (n ¼ 121), we measured dietary iron intake, estimated iron bioavailability and determined body mass index s.d. scores (BMI-SDS). In all children (n ¼ 121), we measured fasting serum ferritin, soluble transferrin receptor (sTfR), C-reactive protein (CRP) and leptin; in a subsample, we measured IL-6 (n ¼ 68) and serum hepcidin (n ¼ 30). Results: There were no significant differences in dietary iron intake or bioavailability comparing normal and overweight children. The prevalence of iron-deficient erythropoiesis (an increased sTfR concentration) was significantly higher in the overweight than in the normal weight children (20 vs 6%, P ¼ 0.022, with sTfR concentrations of 4.40 ± 0.77 and 3.94 ± 0.88 mg l À1 , respectively, P ¼ 0.010). Serum hepcidin levels were significantly higher in the overweight children (P ¼ 0.001). BMI-SDS significantly correlated with sTfR (P ¼ 0.009), serum hepcidin (P ¼ 0.005) and the three measures of subclinical inflammation, namely CRP (Po0.001), IL-6 (Po0.001) and leptin (Po0.001). In a multiple regression model, serum hepcidin was correlated with BMI-SDS (P ¼ 0.020) and body iron (P ¼ 0.029), but not with the inflammatory markers. Conclusion: Our findings indicate that there is reduced iron availability for erythropoiesis in overweight children and that this is unlikely due to low dietary iron supply but rather due to hepcidin-mediated reduced iron absorption and/or increased iron sequestration.

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Section: Discussionsupporting

confidence: 92%

Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children

2009

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“…This is consistent with previous studies in children in industrialized countries [13][14][15][16][17][18] reporting an inverse relationship between iron status and adiposity, For example, in the NHANES III sample of 9698 older US children, where 14% were at risk for overweight, 10% were overweight and 3% were iron deficient, those at risk for overweight and who were overweight were twice as likely to be iron deficient compared to those not overweight. 17 Our data demonstrate this same relationship exists in children in transition countries with higher rates of iron deficiency and lower rates of adiposity.…”

Section: Discussionsupporting

confidence: 92%

“…11 In many lower income countries, the prevalence of overweight is increasing at 2-4 times the rate of the industrialized world. 12 Studies in industrialized countries have consistently found higher rates of iron deficiency in overweight children [13][14][15][16][17][18] and adults. [19][20][21][22][23] Although the mechanism is unclear, this may be due to lower iron intakes and/or increased iron requirements in overweight individuals.…”

Section: Introductionmentioning

confidence: 99%

Adiposity in women and children from transition countries predicts decreased iron absorption, iron deficiency and a reduced response to iron fortification

et al. 2008

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Background: Overweight is increasing in transition countries, while iron deficiency remains common. In industrialized countries, greater adiposity increases risk of iron deficiency. Higher hepcidin levels in obesity may reduce dietary iron absorption. Therefore, we investigated the association between body mass index (BMI) and iron absorption, iron status and the response to iron fortification in populations from three transition countries (Thailand, Morocco and India). Methods: In Thai women (n ¼ 92), we examined the relationship between BMI and iron absorption from a reference meal containing B4 mg of isotopically labeled fortification iron. We analyzed data from baseline (n ¼ 1688) and intervention (n ¼ 727) studies in children in Morocco and India to look for associations between BMI Z-scores and baseline hemoglobin, serum ferritin and transferrin receptor, whole blood zinc protoporphyrin and body iron stores, and changes in these measures after provision of iron. Results: In the Thai women, 20% were iron deficient and 22% were overweight. Independent of iron status, a higher BMI Z-score was associated with decreased iron absorption (P ¼ 0.030). In the Indian and Moroccan children, 42% were iron deficient and 6.3% were overweight. A higher BMI Z-score predicted poorer iron status at baseline (Po0.001) and less improvement in iron status during the interventions (Po0.001). Conclusions: Adiposity in young women predicts lower iron absorption, and pediatric adiposity predicts iron deficiency and a reduced response to iron fortification. These data suggest the current surge in overweight in transition countries may impair efforts to control iron deficiency in these target groups. Interactions of the 'double burden' of malnutrition during the nutrition transition may have adverse consequences.

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“…Human epidemiology studies revealed that elevated levels of ferritin may be an indication of systemic iron overload (Cook et al 1974;Zimmermann 2008) and are positively associated with obesity (Wenzel et al 1962;Gillum 2001;Iwasaki et al 2005) and obesity-related diseases such as diabetes, hypertension, dyslipidaemia, or nonalcoholic fatty liver disease (Jehn et al 2004;Bozzini et al 2005;Mascitelli et al 2009;Dongiovanni et al 2011;Kim et al 2011;see Zafon et al 2010 for review). Precisely why elevations in ferritin levels or systemic iron overload are associated with these conditions is not entirely clear, with potential explanations ranging from excess iron causing oxidative stress, endoplasmic reticulum (ER) stress, inflammation, and dysfunction of adipose tissue (Hubler et al 2015;Nikonorov et al 2015).…”

mentioning

confidence: 99%

Iron Overload Coordinately Promotes Ferritin Expression and Fat Accumulation in Caenorhabditis elegans

Wang¹,

Jiang

et al. 2016

Genetics

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The trace element iron is crucial for living organisms, since it plays essential roles in numerous cellular functions. Systemic iron overload and the elevated level of ferritin, a ubiquitous intracellular protein that stores and releases iron to maintain the iron homeostasis in cells, has long been epidemiologically associated with obesity and obesity-related diseases. However, the underlying mechanisms of this association remain unclear. Here, using Caenorhabditis elegans, we show that iron overload induces the expression of sgk-1, encoding the serum and glucocorticoid-inducible kinase, to promote the level of ferritin and fat accumulation. Mutation of cyp-23A1, encoding a homolog of human cytochrome P450 CYP7B1 that is related to neonatal hemochromatosis, further enhances the elevated expression of ftn-1, sgk-1, and fat accumulation. sgk-1 positively regulates the expression of acs-20 and vit-2, genes encoding homologs of the mammalian FATP1/4 fatty acid transport proteins and yolk lipoproteins, respectively, to facilitate lipid uptake and translocation for storage under iron overload. This study reveals a completely novel pathway in which sgk-1 plays a central role to synergistically regulate iron and lipid homeostasis, offering not only experimental evidence supporting a previously unverified link between iron and obesity, but also novel insights into the pathogenesis of iron and obesity-related human metabolic diseases. KEYWORDS iron; serum and glucocorticoid inducible kinase SGK-1; lipid uptake; obesity; C. elegans D UE to its essential roles in numerous cellular functions across nearly all living organisms, including oxygen transport, electron transport, DNA synthesis, and enzyme catalysis, exploring how iron is stored and regulated has been a growing focus in numerous fields. Dietary iron is absorbed primarily by duodenal enterocytes via the divalent metal-ion transporter 1 (DMT1) after it is reduced at the apical membrane. Subsequently, it is either stored in ferritin, which dynamically regulates iron sequestration, storage, and release or it is transported from enterocytes into the blood stream via the basolateral transporter ferroportin (Fleming and Ponka 2012). Consequently, the total amount of iron in the body is determined by its intake and storage, which are all finely regulated by many factors and signaling pathways at various levels (Fleming and Ponka 2012;Hubler et al. 2015), many of which not entirely understood.Human epidemiology studies revealed that elevated levels of ferritin may be an indication of systemic iron overload (Cook et al. 1974;Zimmermann 2008) and are positively associated with obesity (Wenzel et al. 1962;Gillum 2001;Iwasaki et al. 2005) and obesity-related diseases such as diabetes, hypertension, dyslipidaemia, or nonalcoholic fatty liver disease (Jehn et al. 2004;Bozzini et al. 2005;Mascitelli et al. 2009;Dongiovanni et al. 2011;Kim et al. 2011; see Zafon et al. 2010 for review). Precisely why elevations in ferritin levels or systemic iron overload are associated w...

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Hypoferræmia in Obese Adolescents

Cited by 208 publications

References 8 publications

Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children

Overweight children have higher circulating hepcidin concentrations and lower iron status but have dietary iron intakes and bioavailability comparable with normal weight children

Adiposity in women and children from transition countries predicts decreased iron absorption, iron deficiency and a reduced response to iron fortification

Iron Overload Coordinately Promotes Ferritin Expression and Fat Accumulation in Caenorhabditis elegans

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