Apart from nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H2S) is the third gaseous mediator in mammals. H2S 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, H2S is involved in the regulation of vascular tone and blood pressure, inhibits atherogenesis, and protects myocardium from ischemia-reperfusion injury. Recent studies indicate that H2S 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, H2S inhibits basal and insulin-stimulated glucose uptake in visceral adipose tissue, and may be involved in the pathogenesis of insulin resistance. H2S production in periadventitial adipose tissue is stimulated by vasoconstrictors and aortic banding-induced hypertension and downregulated by aging. H2S signaling in adipose tissue may be affected by pharmacotherapy. Lipid-soluble statins (3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors) increase H2S 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 H2S oxidation.
Adipobiology 2010; 2: 41-50.
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