Carbon Monoxide and the Pancreas

Christian      I. Schwer

doi:10.2174/138920112800399293

Abstract

Carbon monoxide (CO), often referred to as the silent killer, is a colorless, odorless and tasteless gas. It combines with hemoglobin to produce carboxyhemoglobin, which is ineffective for delivering oxygen to animal and human tissues. On the other hand, CO is endogenously produced in the body as a byproduct of heme degradation catalyzed by the heme oxygenase (HO) enzymes. In the past decade, evidence has accumulated to suggest important physiological roles for CO in mammalian tissues. In the pancreas, modulation of endogenous CO production or administration of exogenous CO may represent a therapeutic option for the treatment of endocrine and exocrine pancreatic disorders. In cell culture, CO exerts anti-diabetic effects and brief exposure of purified mouse islets to CO ameliorates functional performance after transplantation. Recent advances include the observation that CO carriers possess potent anti-proliferative effects in an in vitro model of pancreatic fibrosis. In vivo, CO confers tissue protection in animal models of pancreatic disease, including those with hyperglycemia and inflammatory injury of the gland. However, there are still a number of unanswered questions surrounding its physiological and pathophysiological relevance and the preferred route of CO administration in the pancreas still remains to be settled. This brief review focuses on the roles, effects and mechanisms of action of CO in the pancreas.

Keywords: Carbon monoxide, Diabetes, Heme oxygenase, Fibrosis, Nitric oxide, Pancreatitis

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