Table 3. Experimental studies regarding the effects of iron supplementation on energy metabolism in cells.

Model	Design	Phenotype	Ref.
Primary hepatocytes isolated from 5-wk-old male C57BL/6J mice	Treated with 100, 300, and 1,000 μM SFC for 24 hr	• SFC treatment up-regulated the genes related to mitochondrial function, heme, and iron-sulfur clusters	[9]
Primary hepatocytes isolated from male C57BL/6 mice	Treated with 0, 7.5, 75, or 750 μM FAC for 16 hr	• FAC treatment inhibited the expression of acetyl-CoA carboxylase and fatty acid synthase	[60]
AML12 hepatocytes	Treated with 30 μg/mL FAC for 12 (mild group) or 24 hr (moderate group)	• FAC treatment caused an increase in the accumulation of lipids in hepatocytes	[61]
		• The 12 hr (mild group) iron treatment increased lipogenesis of hepatocytes
Primary human hepatocytes	Treated with 50 μM iron for 48 or 72 hr	• The iron treatment caused the accumulation of triglycerides in hepatocytes	[62]
Primary HUVECs	Treated with 100 μM of FAC, FAS, and ferric chloride, 2 mg/mL of apoferritin and holoferritin for 24 hr	• Cellular iron loading caused cholesterol biosynthesis	[63]
Human and mouse 3T3-L1 pre-adipocytes	Treated with 3 and 30 μg/mL FeSO4, 20 and 100 μmol/L deferoxamine for 7 or 14 day	• Transferrin was significantly elevated during adipocyte differentiation	[70]
		• Iron deficiency in cells elevated gene expressions of inflammatory markers and disturbed adipocyte differentiation, which was restored by iron supplementation in a dose-dependent way
		• Palmitic acid treatment induced iron deficiency during adipocyte differentiation, and led to a decrease in the transferrin gene expression, which was restored by the treatment of transferrin

FAC, ferric ammonium citrate; FAS, ferrous ammonium sulfate; HUVEC, human umbilical vein endothelial cell; SFC, sodium ferrous citrate; acetyl-CoA, acetyl coenzyme A.