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Our data demonstrate that lack of VDR signaling in endothelial cells leads to a state of endothelial activation with increased leukocyte-endothelial cell interactions that may contribute to the more severe plaque accumulation observed in apoE -/-VDR -/- mice. apoE -/-VDR -/-mice showed higher aortic expression of VCAM-1, ICAM-1 and IL-6 when compared to apoE -/-VDR +/+ mice. In vivo, deletion of VDR led to significantly larger aortic arch and aortic root lesions in apoE -/- mice, with higher macrophage content. Inhibition of NF-κB activation with super-repressor IκBα blunted all signs of endothelial cell activation caused by downregulation of VDR in endothelial cells. shVDR cells showed decreased IκBα levels and accumulation of p65 in the nucleus compared to shRNA controls. Knockdown of VDR in endothelial cells (shVDR) led to endothelial cell activation, characterized by upregulation of VCAM-1, ICAM-1 and IL-6, decreased peripheral blood mononuclear cell (PBMC) rolling velocity and increased PBMC rolling flux and adhesion to the endothelium. Our aim was to assess the role of basal levels of vitamin D receptor (VDR) on the early leukocyte recruitment and related endothelial cell-adhesion-molecule expression, as essential prerequisites for the onset of atherosclerosis. Vitamin D has cardioprotective actions, while its deficiency is a risk factor for the progression of cardiovascular damage. Coauthors are from UNC Chapel Hill and the University of California, Davis.Endothelial cell activation leading to leukocyte recruitment and adhesion plays an essential role in the initiation and progression of atherosclerosis. Support came from the Environmental Protection Agency and the National Institute of Environmental Health Sciences. The research appears in Scientific Reports. While we don’t yet understand the mechanism, we are beginning to tease that out.”įuture work will involve looking at the offspring of vitamin D deficient mothers, to determine whether this vitamin deficiency has epigenetic effects that can be passed down. “Somehow the energy that should be going toward growth is getting shunted into creating fat and lipids, and this occurrence cannot be easily reversed. “This work shows that vitamin D deficiency can influence metabolic health by disrupting the normal balance between growth and fat accumulation,” Kullman says. While the fish did continue to grow and begin to utilize fat reserves, they never caught up in size with the other cohorts and they retained residual fat deposits. This, combined with the stunted growth, indicates that vitamin D plays an important role in the ability to channel energy into growth versus into fat storage.”Īfter the initial testing, the vitamin D deficient zebrafish were given a vitamin D enriched diet for an additional six months, to see if the results could be reversed. “They also had higher triglycerides and cholesterol, which are hallmarks of metabolic imbalance that can lead to cardio-metabolic disease. “The vitamin D deficient zebrafish exhibited both hypertrophy and hyperplasia-an increase in both the size and number of fat cells,” Kullman says. The zebrafish in the vitamin D deficient group were, on average, 50% smaller than those in the other two groups, and they had significantly more fat reserves. They also examined key metabolic pathways associated with fat production, storage, and mobilization and growth promotion. The zebrafish spent four months on their particular diet, then the researchers looked at their growth, bone density, triglyceride, lipid, cholesterol, and vitamin D levels. The research team, led by Seth Kullman, professor of biological sciences at North Carolina State University, looked at groups of post-juvenile zebrafish on one of three diets: no vitamin D (or vitamin D null), vitamin D enriched, and control. The results suggest a link between vitamin D and metabolic homeostasis, or equilibrium.
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Vitamin D deficiency during the early development of zebrafish can disrupt the metabolic balance between growth and fat accumulation, research finds. University North Carolina State University