Abstract
Nitric oxide (NO) and hydrogen sulfide (H(2)S) are two gasotransmitters that are produced in the human body and have a key role in many of the physiological activities of the various organ systems. Decreased NO bioavailability and deficiency of H(2)S are involved in the pathophysiology of type 2 diabetes and its complications. Restoration of NO levels have favorable metabolic effects in diabetes. The role of H(2)S in pathophysiology of diabetes is however controversial; H(2)S production is decreased during development of obesity, diabetes, and its complications, suggesting the potential therapeutic effects of H(2)S. On the other hand, increased H(2)S levels disturb the pancreatic β-cell function and decrease insulin secretion. In addition, there appear to be important interactions between NO and H(2)S at the levels of both biosynthesis and signaling pathways, yet clear an insight into this relationship is lacking. H(2)S potentiates the effects of NO in the cardiovascular system as well as NO release from its storage pools. Likewise, NO increases the activity and the expression of H(2)S-generating enzymes. Inhibition of NO production leads to elimination/attenuation of the cardioprotective effects of H(2)S. Regarding the increasing interest in the therapeutic applications of NO or H(2)S-releasing molecules in a variety of diseases, particularly in the cardiovascular disorders, much is to be learned about their function in glucose/insulin metabolism, especially in diabetes. The aim of this review is to provide a better understanding of the individual and the interactive roles of NO and H(2)S in carbohydrate metabolism.