Title:Carbon Monoxide and the Pancreas
VOLUME: 13 ISSUE: 6
Author(s):Christian I. Schwer
Affiliation:Department of Anesthesiology and Critical Care Medicine, University Medical Center, Hugstetter Strasse 55, D-79106 Freiburg, Germany.
Keywords:Carbon monoxide, Diabetes, Heme oxygenase, Fibrosis, Nitric oxide, Pancreatitis
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.
