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.
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In this study, we investigated the associations of maternal dietary iron intake during the first trimester of pregnancy and pregnancy outcomes and related complications in pregnant women of Isfahan, Iran. In this prospective study, 812 healthy first-trimester singleton pregnant women were selected randomly from 20 various health centers across Isfahan city during 2015–2016. The maternal dietary iron classified into 2 groups, including heme and non-heme iron. Factors including pre-eclampsia, gestational hypertension, gestational diabetes mellitus, intrauterine growth restriction (IUGR), and nausea and vomiting in pregnancy considered as the pregnancy-related complications. Infant's birth weight, birth height, and birth head circumference were also determined as the pregnancy-outcomes. There was a significant association between total iron consumption and infant head circumference (p = 0.01). Total maternal iron (the sum of heme and non-heme iron) was negatively associated with both infant's birth height (p = 0.006) and birth weight (p = 0.02). Non-heme iron consumption is positively associated with high-risk of IUGR (p = 0.004). Heme intake was associated with an increased risk of maternal fasting blood sugar (FBS) (p = 0.04). Higher heme, non-heme, and total iron intake were associated with lower risk of pre-eclampsia (heme: crude p = 0.05; non-heme iron: adjusted p = 0.02; total iron: adjusted p = 0.05). Maternal total iron intake was directly associated with infant head circumference, whereas, negatively associated with both birth weight and birth height. High non-heme iron intake may increase the risk of IUGR, and a high intake of heme iron may increase FBS.
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