Michael Ristow, Hindrik Mulder, Doreen Pomplun, Tim J. Schulz, Katrin Müller-Schmehl, Anja Krause, Malin Fex, Hélène Puccio, Jörg Müller, Frank Isken, Joachim Spranger, Dirk Müller-Wieland, Mark A. Magnuson, Matthias Möhlig, Michel Koenig, Andreas F.H. Pfeiffer
J Clin Invest.
2003;
112(4):527–534
doi:10.1172/JCI18107
This article Copyright © 2003, The American Society for Clinical Investigation
Abstract
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D
iabetes is caused by an absolute (type 1) or relative (type 2) deficiency of insulin-producing β cells. We have disrupted expression of the mitochondrial protein frataxin selectively in pancreatic β cells. Mice were born healthy but subsequently developed impaired glucose tolerance progressing to overt diabetes mellitus. These observations were explained by impairment of insulin secretion due to a loss of β cell mass in knockout animals. This phenotype was preceded by elevated levels of reactive oxygen species in knockout islets, an increased frequency of apoptosis, and a decreased number of proliferating β cells. Hence, disruption of the frataxin gene in pancreatic β cells causes diabetes following cellular growth arrest and apoptosis, paralleled by an increase in reactive oxygen species in islets. These observations might provide insight into the deterioration of β cell function observed in different subtypes of diabetes in humans.
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