Carbon monoxide and ?-cell function: Implications for type 2 diabetes mellitus

Carbon monoxide (CO), a member of the multifunctional gasotransmitters family produced by heme oxygenases (i.e., HO-1 and HO-2), has received significant attention because of its involvement in carbohydrate metabolism. Experimental evidence indicates that both HO-2- and HO-1-derived CO stimulate insulin secretion, but the latter mainly acts as a compensatory response in pre-diabetes conditions. CO protects pancreatic I3-cell against cytokine- and hypoxia-induced apoptosis and promotes I3-cell regeneration. CO cross-talks with nitric oxide (NO) and hydrogen sulfide (H2S), other important gasotransmitters in carbohydrate metabolism, in regulating I3-cell function and insulin secretion. These data speak in favor of the potential therapeutic application of CO in type 2 diabetes mellitus (T2DM) and preventing the progression of pre-diabetes to diabetes. Either CO (as both gaseous form and CO-releasing molecule) or pharmacological formulations made of natural HO inducers (i.e., bioactive components originating from plant-based foods) are potential candidates for developing CO-based therapeutics in T2DM. Future studies are needed to assess the safety/efficacy and potential therapeutic applications of CO in T2DM.

Automated summary

Carbon monoxide (CO) plays a significant role in carbohydrate metabolism by stimulating insulin secretion, protecting pancreatic β-cells, and interacting with other gasotransmitters such as nitric oxide and hydrogen sulfide. Therefore, CO may have potential therapeutic applications in treating type 2 diabetes mellitus and preventing the progression of prediabetes.