This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lin, J.-M. Articles by Bergsten, P. Search for Related Content PubMed PubMed Citation Articles by Lin, J.-M. Articles by Bergsten, P.

Preserved Pulsatile Insulin Release from Prediabetic Mouse Islets¹

Department of Medical Cell Biology, Uppsala University, SE-751 23 Uppsala, Sweden

Address all correspondence and requests for reprints to: Dr. Peter Bergsten, Department of Medical Cell Biology, Uppsala University, Box 571, SE-751 23 Uppsala, Sweden. E-mail: Peter.Bergsten{at}medcellbiol.uu.se

During the development of type I diabetes, the plasma insulin pattern changes. Because the islet secretory pattern has been implicated in this phenomenon, insulin release was measured from female nonobese diabetic (NOD) mouse islets isolated at different ages. Islets from 5-week-old mice were used as controls because they had no infiltrating mononuclear cells and insulin release rose almost 9-fold with maintained oscillatory frequency when the glucose concentration was raised from 3 to 11 mM. Islets isolated from 13- and 25-week-old mice were infiltrated with mononuclear cells. In these islets, increase in the glucose concentration from 3 to 11 mM only doubled insulin release. However, despite the cellular infiltration, insulin release was pulsatile. Islets from 13-week-old mice had reduced glucose oxidation rate. Culture of such islets for 7 days at 11.1 mM glucose causes a decrease in the number of mononuclear cells infiltrating the islets, which in the present study was accompanied by a normalization of both glucose oxidation and glucose-induced insulin release. In the presence of the mitochondrial substrate -keto-isocaproate (5 mM) both control and infiltrated islets responded with pronounced insulin pulses with similar amplitudes. The results suggest that the deranged plasma insulin pattern observed during the development of type I diabetes may be related to decrease in the insulin pulse amplitude rather than loss of the pulsatile release from the islets.

This article has been cited by other articles:

				S. M. Katzman, M. A. Messerli, D. T. Barry, A. Grossman, T. Harel, J. D. Wikstrom, B. E. Corkey, P. J. S. Smith, and O. S. Shirihai Mitochondrial metabolism reveals a functional architecture in intact islets of Langerhans from normal and diabetic Psammomys obesus Am J Physiol Endocrinol Metab, December 1, 2004; 287(6): E1090 - E1099. [Abstract] [Full Text] [PDF]

				J.-M. Lin, M. E. Fabregat, R. Gomis, and P. Bergsten Pulsatile Insulin Release From Islets Isolated From Three Subjects With Type 2 Diabetes Diabetes, April 1, 2002; 51(4): 988 - 993. [Abstract] [Full Text] [PDF]

				J. Westerlund and P. Bergsten Glucose Metabolism and Pulsatile Insulin Release From Isolated Islets Diabetes, August 1, 2001; 50(8): 1785 - 1790. [Abstract] [Full Text] [PDF]