Hydrogen sulfide: synthesis and function in the adipose tissue

Abstract

Apart from nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H 2 S) is the third gaseous mediator in mammals. H 2 S is synthesized from L-cysteine by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), or by sequential action of alanine aminotransferase and 3-mercaptopyruvate sulfurtransferase. In the cardiovascular system, H 2 S is involved in the regulation of vascular tone and blood pressure, inhibits atherogenesis, and protects myocardium from ischemia-reperfusion injury. Recent studies indicate that H 2 S is synthesized also in the adipose tissue. Hydrogen sulfide produced in periadventitial adipose tissue (tunica adiposa) of the blood vessels induces vasodilation by activating K + channels in smooth muscle cells. On the other hand, H 2 S inhibits basal and insulin-stimulated glucose uptake in visceral adipose tissue, and may be involved in the pathogenesis of insulin resistance. H 2 S production in periadventitial adipose tissue is stimulated by vasoconstrictors and aortic banding-induced hypertension and downregulated by aging. H 2 S signaling in adipose tissue may be affected by pharmacotherapy. Lipid-soluble statins (3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors) increase H 2 S level in periadventitial adipose tissue and thus augment its anticontractile effect on the blood vessels. This effect of statins results from the depletion of ubiquinone - a component of mitochondrial respiratory chain - and the impairment of mitochondrial H 2 S oxidation. Adipobiology 2010; 2: 41-50.