Riboflavin Deficiency Alters Cholesterol Homeostasis Partly by Reducing Apolipoprotein B100 Synthesis in HepG2 Cells

Riboflavin deficiency led to lower blood cholesterol level and higher content of hepatic cholesterol in rats and the mechanisms are not clarified yet. We hypothesized that riboflavin deficiency might alter cholesterol homeostasis via apolipoprotein B100, one of the important proteins in cholesterol transport. To test this hypothesis, HepG2 cells were cultured in riboflavin-deficient media for 4 days to develop riboflavin deficiency. Compared to riboflavin-sufficient cells, the mRNA (0. 37 ± 0.04 vs 1.03 ± 0.29 relative expression level, n = 3) and protein expressions of apolipoprotein B100 (intracellular: 173.7 ± 14.4 vs 254.8 ± 47.2 μg/mg protein; extracellular: 93.8 ± 31.1 vs 161.6 ± 23.9 μg/mg protein; n = 3) were significantly reduced in riboflavin-deficient cells ( P < 0.05). Endoplasmic reticulum oxidoreductin 1 and protein disulfide isomerase, two enzymes involved in the oxidative folding of apolipoprotein B100, were also lower remarkably in expression at both mRNA and protein levels. Meanwhile, intracellular cholesterol was increased (256.3 ± 17.1 μM/g protein vs 181.4 ± 23.9 μM/g protein, n = 4) and extracellular cholesterol decreased (110.0 ± 23.2 μM/g protein vs 166.2 ± 34.6 μM/g protein, n = 4) significantly in riboflavin-deficient cells ( P < 0.05). Very low-density lipoprotein was also diminished (29.0 ± 6.1 μM/g protein vs 67.0 ± 11.0 μM/g protein, n = 4) in the culture media ( P < 0.05). These findings suggest that riboflavin deficiency alters cholesterol homeostasis partly by reducing apolipoprotein B100 synthesis in HepG2 cells.

Vitamin B2 (riboflavin) in pregnancy and breastfeeding

Riboflavin is a cofactor for enzymes involved in energy generation, biosynthesis, detoxification, and electron-scavenging pathways, as well as in the metabolism of other B vitamins. Deficiency is rare in developed countries; it is encountered almost invariably in combination with deficit of other B vitamins in areas of poor overall nutrition. Deficiency is endemic in populations whose staple diet consists of rice and wheat, with low or no consumption of meat and dairy products. Infants of riboflavin-deficient mothers tend to be deficient themselves at birth and remain deficient through breastfeeding and weaning. To ensure adequate riboflavin supply in both mother and infant, an increase in dairy products and/or meat consumption, particularly during lactation, may be necessary in some women.