Dietary advice is the cornerstone in first-line treatment of metabolic diseases. Nutritional interventions directed at these clinical conditions mainly aim to (a) improve insulin resistance by reducing energy-dense macronutrient intake to obtain weight loss and (b) reduce fluctuations in insulin secretion through avoidance of rapidly absorbable carbohydrates. However, even in the majority of motivated patients selected for clinical trials, massive efforts using this approach have failed to achieve lasting efficacy. Less attention has been given to the role of micronutrients in metabolic diseases. Here, we review the evidence that highlights (a) the importance of iron in pancreatic beta-cell function and dysfunction in diabetes and (b) the integrative pathophysiological effects of tissue iron levels in the interactions among the beta cell, gut microbiome, hypothalamus, innate and adaptive immune systems, and insulin-sensitive tissues. We propose that clinical trials are warranted to clarify the impact of dietary or pharmacological iron reduction on the development of metabolic disorders.

Iron Regulation of Pancreatic Beta-Cell Functions and Oxidative Stress.

Working group reports: evaluation of the evidence to support practice guidelines for nutritional care of preterm infants—the Pre-B Project

Background Prenatal alcohol exposure (PAE) causes neurodevelopmental disabilities, and gestational iron deficiency (ID) selectively worsens learning and neuroanatomical and growth impairments in PAE. It is unknown why ID worsens outcomes in alcohol-exposed offspring. Objective We hypothesized that PAE alters maternal-fetal iron distribution or its regulation. Methods Nulliparous, 10-wk-old, Long-Evans rats were mated and then fed iron-sufficient (100 mg Fe/kg) or iron-deficient (≤4 mg Fe/kg) diets. On gestational days 13.5-19.5, dams received either 5.0 g ethanol/kg body weight (PAE) or isocaloric maltodextrin by oral gavage. On gestational day 20.5, maternal and fetal clinical blood counts, tissue mineral and iron transport protein concentrations, and hepatic hepcidin mRNA expression were determined. Results In fetal brain and liver (P 300% (P Conclusions PAE altered fetal iron distribution independent of maternal iron status in rats. The elevated iron content of fetal liver suggests that PAE may have limited iron availability for fetal erythropoiesis and brain development. Altered fetal iron distribution may partly explain why maternal ID substantially worsens growth and behavioral outcomes in PAE.

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Prenatal Alcohol Exposure Alters Fetal Iron Distribution and Elevates Hepatic Hepcidin in a Rat Model of Fetal Alcohol Spectrum Disorders

Respiratory disease accounts for a large proportion of emergency admissions to hospital and diseaseassociated mortality. Genetic association studies demonstrate a link between iron metabolism and pulmonary disease phenotypes. IREB2 is a gene that produces iron regulatory protein 2 (IRP2), which has a key role in iron homeostasis. This review addresses pathways involved in iron metabolism, particularly focusing on the role of IREB2. In addition to this, environmental factors also influence phenotypic variation in respiratory disease, for example inhaled iron from cigarette smoke is deposited in the lung and causes tissue damage by altering iron homeostasis. The effects of cigarette smoke are detailed in this article, particularly in relation to lung conditions that favour the upper lobes, such as emphysema and lung cancer. Clinical applications of iron homeostasis are also discussed in this review, especially looking at the pathophysiology of chronic obstructive pulmonary disease, lung cancer, pulmonary infections and acute respiratory distress syndrome. Promising new treatments involving iron are also covered.

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The role of iron in pulmonary pathology.

To estimate the effect of tobacco smoking on iron homeostasis and the possible association between hepcidin and the neonatal birth weight and length, concentrations of serum hepcidin and selected iron markers were measured in 81 healthy pregnant women (41 smokers and 40 nonsmokers). The smoking mothers had significantly lower concentrations of serum hepcidin (p < 0.001), iron (p < 0.001), and hemoglobin (p < 0.05), but higher erythropoietin (p < 0.05) levels compared with non-smoking pregnant women. Logistic regression analysis showed the highest negative impact of the number of cigarettes smoked per day (β = −0.46; p < 0.01) and positive impact of ferritin level (β = 0.47; p < 0.001) on serum hepcidin concentration. The birth weight and the body length of smoking mothers’ infants were significantly lower than in tobacco abstinent group (p < 0.001). In multiple regression analysis, birth body weight (β = 0.56; p < 0.001) and length (β = 0.50; p < 0.001) were significantly related to maternal hepcidin values. Tobacco smoking affected hepcidin level in serum of pregnant women in a dose-dependent manner. Low concentrations of iron and hemoglobin in maternal serum coexisting with high level of erythropoietin suggest that smoking could lead to subclinical iron deficiency and chronic hypoxia not only in mothers but also in fetus. Low serum hepcidin concentration in smoking pregnant women might be associated with lower fetal birth weight and length.

/pdf/hepcidin-and-iron-metabolism-in-pregnancy-correlation-with-7l08ujfodf.pdf

Hepcidin and Iron Metabolism in Pregnancy: Correlation with Smoking and Birth Weight and Length

Background Maternal smoking has been known to have a negative impact on the well being of the developing fetus. Prenatal smoking has been associated with premature births, low birth weight and with certain birth defects. Small research studies have also found a negative correlation between maternal smoking and neonatal body iron. Objectives To study and compare the relationship between maternal and infants' body iron in smokers and non-smokers in a large matched-pair cohort. Methods This was a prospective cohort study involving 144 mothers - 72 smokers and 72 non-smokers and their respective infants. Samples were obtained from maternal and infants' cord blood at delivery for Serum transferrin receptor (sTfR) and ferritin levels. Serum TfR and ferritin were measured by RAMCO ELISA and RIA assays. Total Body Iron (TBI) was calculated using the sTfR/ferritin ratio in a previously described formula by Cook et al. Results Women who smoked had lower sTfR, higher ferritin and higher body iron compared to nonsmoking women. In contrast to their respective mothers, we found a small, but statistically significant negative correlation between smoking and infants' total body iron. The number of packs per day smoked was also negatively correlated with infants' ferritin and total body iron. Lower birth weight was noted in babies of smokers compared to nonsmokers (mean /- SD =3270 +/-475 vs. 3393 g +/- 475 g, p=0.03). Conclusion Women who smoked during pregnancy had higher iron stores but their newborn infants had lower iron stores than those of non-smoking mothers. The more packs per day (PPD) and more days smoked during pregnancy led to lower total body iron of the babies. There may be a negative dose-dependent response between fetal smoke exposure and infant iron stores.

https://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1019&context=fshn_hs_pubs

Effect of Maternal Cigarette Smoking on Newborn Iron Stores.

Effect Of Maternal Cigarette Smoking On Newborn Iron Stores

Background: Maternal smoking has been known to have a negative impact on the well being of the developing fetus. Prenatal smoking has been associated with premature births, low birth weight and with certain birth defects. Small research studies have also found a negative correlation between maternal smoking and neonatal body iron. Objectives: To study and compare the relationship between maternal and infants’ body iron in smokers and non-smokers in a large matched-pair cohort. Methods: This was a prospective cohort study involving 144 mothers – 72 smokers and 72 non-smokers and their respective infants. Samples were obtained from maternal and infants’ cord blood at delivery for Serum transferrin receptor (sTfR) and ferritin levels. Serum TfR and ferritin were measured by RAMCO ELISA and RIA assays. Total Body Iron (TBI) was calculated using the sTfR/ferritin ratio in a previously described formula by Cook et al. Results: Women who smoked had lower sTfR, higher ferritin and higher body iron compared to nonsmoking women. In contrast to their respective mothers, we found a small, but statistically significant negative correlation between smoking and infants’ total body iron. The number of packs per day smoked was also negatively correlated with infants’ ferritin and total body iron. Lower birth weight was noted in babies of smokers compared to nonsmokers (mean /- SD=3270 +/-475 vs. 3393 g +/- 475 g, p=0.03). Conclusion: Women who smoked during pregnancy had higher iron stores but their newborn infants had lower iron stores than those of non-smoking mothers. The more packs per day (PPD) and more days smoked during pregnancy led to lower total body iron of the babies. There may be a negative dose-dependent response between fetal smoke exposure and infant iron stores.

Jakica Tancabelic

Papers

Effect of Maternal Cigarette Smoking on Newborn Iron Stores.

Effect Of Maternal Cigarette Smoking On Newborn Iron Stores

Effect of maternal cigarette smoking on newborn iron