Vitamin D improves vascular function and decreases monoamine oxidase A expression in experimental diabetes.

The active form of vitamin D, 1,25-dihydroxycholecalciferol (1,25(OH)D), was reported to improve vascular function in patients with diabetes, yet the underlying mechanisms remain to be fully elucidated. Monoamine oxidase (MAO), a mitochondrial enzyme, with two isoforms (A and B) that generates hydrogen peroxide (HO) as by-product, has been recently reported to contribute to the pathogenesis of endothelial dysfunction in diabetes. The present study assessed the interaction between vitamin D and MAO in the vascular wall in the setting of type 1 experimental diabetes.

Monoamine oxidase inhibition improves vascular function and reduces oxidative stress in rats with lipopolysaccharide-induced inflammation.

Oxidative stress and vascular inflammation are the two major pathomechanisms that contribute to the progression of both cardiovascular and metabolic diseases. We have previously demonstrated that monoamine oxidases (MAOs), mitochondrial enzymes with two isoforms (A and B), are contributors to the endothelial dysfunction associated with inflammation in mice. The present study was purported to assess the effects of MAOs on endothelial dysfunction in rats with lipopolysaccharide (LPS)-induced acute inflammation.