Vitamin D3 (Cholecalciferol) Boosts Hydrogen Sulfide Tissue Concentrations in Heart and other Mouse Organs

Decreased Cystathionine-γ-lyase (CSE) Activity in Livers of Type 1 Diabetic Rats and Peripheral Blood Mononuclear Cells (PBMC) of Type 1 Diabetic Patients

“…Vitamin D supplementation has been found to up-regulate the tissue concentration of H 2 S (55). This study provided evidence that vitamin D supplementation up-regulates both CSE protein expression as well as its activity in either HG-or HG ϩ AA-treated PBMC isolated from healthy individuals, which may up-regulate the tissue concentration of H 2 S as reported previously in studies of vitamin D-supplemented mice (55).…”

“…Vitamin D supplementation decreases blood glucose levels and HbA 1C in both type 2 and type 1 diabetic patients (53,54). Vitamin D supplementation has been found to up-regulate the H 2 S tissue concentration in mouse brain, heart, and kidney tissues (55). Fig.…”

Recent Development of Hydrogen Sulfide Releasing/Stimulating Reagents and Their Potential Applications in Cancer and Glycometabolic Disorders

“…In fact, H 2 S can exert some coincident effects in the body with VD. Notably, Wilinski et al (2012) found that cholecalciferol, also known as VD 3 , could increase tissue H 2 S concentration in mouse heart, brain and kidney. Meanwhile, another report suggested that VD 3 had ability to upregulate glucose transporter type 4 (GLUT4) and decreased glycemia in diabetes through induction of CSE expression and H 2 S generation ( Manna and Jain, 2012 ).…”

Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis

“…MicroRNA (miRNA) controls gene expression at the posttranscriptional level [34] and is one of the main factors involved in the upregulation of CSE expression [16]. Interestingly, currently used drugs, including angiotensinconverting enzyme (ACE) inhibitors (e.g., ramipril) [35], statins [36], calcium channel antagonists (e.g., amlodipine) [37], digoxin [38], vitamin D 3 [39], aspirin [40], metformin [40], and others [23], may increase the production of H 2 S. For example, statins can increase H 2 S synthesis via Aktmediated upregulation of CSE [36] or suppress H 2 S degradation by decreasing the concentration of coenzyme Q, which is a sulfide quinone reductase cofactor [41]. It is worth noting that either exogenously supplied or endogenously produced H 2 S can be stored in the body in the form of bound sulfane, which is a reductant labile sulfur (e.g., persulfide (R-S-S-SH), polysulfide (RSS n SR), and protein-associated sulfur, among others) [42].…”