Nutritional B vitamin deficiency disrupts lipid metabolism causing accumulation of proatherogenic lipoproteins in the aorta adventitia of ApoE null mice
Article first published online: 18 MAY 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Special Issue: Nutrition and Atherosclerosis
Volume 56, Issue 7, pages 1122–1130, July 2012
How to Cite
McNeil, C. J., Beattie, J. H., Gordon, M.-J., Pirie, L. P. and Duthie, S. J. (2012), Nutritional B vitamin deficiency disrupts lipid metabolism causing accumulation of proatherogenic lipoproteins in the aorta adventitia of ApoE null mice. Mol. Nutr. Food Res., 56: 1122–1130. doi: 10.1002/mnfr.201100694
- Issue published online: 4 JUL 2012
- Article first published online: 18 MAY 2012
- Manuscript Accepted: 5 MAR 2012
- Manuscript Revised: 2 MAR 2012
- Manuscript Received: 17 OCT 2011
- Scottish Government Rural and Environment Science and Analytical Services Division
- B vitamin deficiency in ApoE null mice;
- Lipid metabolism;
- Vascular lipid deposition
Cardiovascular disease is the major cause of death in the world. Low dietary folate, elevated homocysteine, and high circulating cholesterol are risk factors.
Methods and results
We investigated whether folate and/or B vitamin deficiency would change lipoprotein and fatty acid metabolism and lipid accumulation in the aorta adventitia of ApoE null mice. Mice (n = 10 per group) were fed a control (C; 4%) or high saturated fat (HF; 21%), and high cholesterol (0.15%) diet for 16 weeks. Folate (F-) or folate, B6 and B12 deficiency (F-B-) were imposed on these diets. Feeding a HF diet increased plasma and liver total cholesterol and HDL cholesterol (two- to threefold; p < 0.05). Total cholesterol increased (twofold; p < 0.05) in aorta adventitial lipid in response to HF. Feeding a diet depleted of folate and B vitamins (F-B-) significantly increased cholesterol accumulation in both liver and aorta adventitial lipid (approximately 50–70%; p < 0.05). Moreover, the proportions of fatty acids in hepatic and adventitial lipid was significantly changed by B vitamin depletion, measured as an increase in saturated fatty acids (approximately 15%) and a decrease (approximately 11%) in monounsaturated fatty acids (p < 0.05).
B vitamin deficiency perturbs lipid metabolism in ApoE null mice, causing accumulation of proatherogenic cholesterol and fatty acids in the aorta adventitia.