Abstract 650: Folic Acid and Vitamin B12 Deficiencies are Cardiovascular Disease Risk Factors Which Can Be Prevented by the Recruitment of the Wnt10b Signaling Pathway
Introduction: Studies have shown that there is a deficiency of folate and vitamin B12 in obese individuals compared with normal BMI controls. Folic acid reduces oxidative stress while vitamin B12 protects against superoxide injuries in endothelial cells. This suggests that increased levels of folate and vitamin B12 might attenuate vascular disease.
Objective: We examined the hypothesis that folic acid and vitamin B12 regulate mesenchymal stem cell-derived adipocytes by up-regulating Wnt10b and heme oxygenase-1 (HO-1), thereby promoting the growth of small healthy adipocytes and reducing the number of large inflamed adipocytes.
Methods: Human bone marrow-derived mesenchymal stem cells were used as a source of adipocytes. MSC-derived adipocytes were treated with either vehicle or one of four concentrations (0.1, 1.0, 10, or 100 μM) of either folic acid or vitamin B12. SiRNA of Wnt10b, DKK-1, and other related genes were also studied.
Results: There was a decrease in adipocytes in a concentration-dependent manner with an optimal level of 10 μM (p<0.05) in both folic acid and vitamin B12 treatment. Treatment of folic acid (10 μM) and vitamin B12 (10 μM) resulted in a decrease in the number of large, unhealthy adipocytes when analyzed using ImagePro Analyzer (p<0.05). The beneficial effects of folic acid and vitamin B12 were reversed when cells were treated with siRNA Wnt10b (p<0.05). The folic acid- and vitamin B12-mediated decreases in adipocyte differentiation were additionally prevented by protein siRNAs including HO-1 (p<0.05).
Conclusion: These novel results demonstrate that increased levels of both folic acid and vitamin B12 attenuate adiposity via significant increases in Wnt10b and related proteins. Folic acid and vitamin B12 supplementation is deemed viable in the prevention and treatment of obesity and obesity-associated diseases.
- © 2012 by American Heart Association, Inc.