Figure 3. Schematic diagram regarding the role of iron in regulating energy metabolism in beige and brown adipocytes. Irons are transferred to the mitochondria for synthesizing iron-sulfur clusters and heme. Excess irons are stored in the form of ferritin or exported through FPN. Iron-sulfur cluster is a component of mitochondrial complexes I, II, and III, and aconitase, and heme is a component of Cyt c. When iron is deficient, thermogenesis-related genes such as PRDM 16, PPAR, PGC1-alpha, and UCP1 are down-regulated.
FPN, ferroportin; Cyt c, cytochrome c; PRDM, PRD1-BF1-RIZ1 homologous domain containing; PPAR, peroxisome proliferator-activated receptor; PGC, peroxisome proliferator-activated receptor-gamma coactivator; UCP, uncoupling protein; ALA, aminolevulinic acid; ALAS, aminolevulinic acid synthase; ISCU, iron-sulfur cluster assembly enzyme; NFS1, cysteine desulfurase; RXR, retinoid X receptor; TCA, tricarboxylic acid; ZFP 516, zinc-finger protein 516; acetyl-CoA, acetyl coenzyme A; FADH2, flavin adenine dinucleotide; NADH, nicotinamide adenine dinucleotide.