Vitamin D and Its Role in the Lipid Metabolism and the Development of Atherosclerosis

Abstract

Vitamin D, a crucial hormone in the homeostasis and metabolism of calcium bone, has lately been found to produce effects on other physiological and pathological processes genomically and non-genomically, including the cardiovascular system. While lower baseline vitamin D levels have been correlated with atherogenic blood lipid profiles, 25(OH)D supplementation influences the levels of serum lipids in that it lowers the levels of total cholesterol, triglycerides, and LDL-cholesterol and increases the levels of HDL-cholesterol, all of which are known risk factors for cardiovascular disease. Vitamin D is also involved in the development of atherosclerosis at the site of the blood vessels. Deficiency of this vitamin has been found to increase adhesion molecules or endothelial activation and, at the same time, supplementation is linked to the lowering presence of adhesion surrogates. Vitamin D can also influence the vascular tone by increasing endothelial nitric oxide production, as seen in supplementation studies. Deficiency can lead, at the same time, to oxidative stress and an increase in inflammation as well as the expression of particular immune cells that play a pivotal role in the development of atherosclerosis in the intima of the blood vessels, i.e., monocytes and macrophages. Vitamin D is also involved in atherogenesis through inhibition of vascular smooth muscle cell proliferation. Furthermore, vitamin D deficiency is consistently associated with cardiovascular events, such as myocardial infarction, STEMI, NSTEMI, unstable angina, ischemic stroke, cardiovascular death, and increased mortality after acute stroke. Conversely, vitamin D supplementation does not seem to produce beneficial effects in cohorts with intermediate baseline vitamin D levels.

Complement Component C1q as a Potential Diagnostic Tool for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Subtyping

“…Other combinations, such as vitamin D deficiency and increment of C1q, or increased LDL with C1q or cholesterol involved over 20% of the participants (>50 cases). Since vitamin D reference values are widely influenced by genetic and environmental factors, and the assays to quantitate its levels typically show variability over ±10% [ 20 , 21 ], leading to a lack of consensus global reference values [ 22 , 23 ], we decided to exclude this variable from our stratified downstream analysis.…”

“…Similarly, since differences found in LDL and cholesterol are nonspecifically associated with disease, sometimes appearing together with vitamin D deficiency [22,23], they were not further pursued, meaning that they were not used to set stratification conditions of our cohort. The unexpected finding of a quite significant proportion of ME/CFS cases showing increased levels of C1q and decreased C1 inhibitor (42.8% and 8.8%, respectively) (Supplementary Table S1), together with the C1q deficiency being associated with autoimmune diseases such as systemic lupus erythematosus [24], motivated our interest to hypothesize C1q as a potential biomarker for ME/CFS subtyping.…”

Impact of Dietary Lipids on the Reverse Cholesterol Transport: What We Learned from Animal Studies

“…Although the impact of liposoluble vitamins and their precursors and metabolites on atherosclerotic cardiovascular disease has been well established in humans [ 55 , 184 , 185 ] and animal models [ 185 ], their role in in vivo m-RCT is less characterized.…”

Preparation and Antioxidant Activity of Chitosan Dimers with Different Sequences

“…A high concentration of reactive oxygen species can damage proteins, lipids and DNA, which leads to oxidative stress, an imbalanced state in the body [ 1 , 2 , 3 ]. Oxidative stress is a major reason for the initiation and progression of many diseases, including cardiovascular diseases [ 4 ], Parkinson’s disease [ 5 ], atherogenesis [ 6 ], neurodegeneration [ 7 ] and cancer [ 8 ]. Antioxidants can scavenge free radicals or retard the progress of many chronic diseases as well as lipid peroxidation.…”