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Am J Physiol Endocrinol Metab 277: E521-E528, 1999;
0193-1849/99 $5.00
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Vol. 277, Issue 3, E521-E528, September 1999

EPILOGUE
Lipid rather than glucose metabolism is implicated in altered insulin secretion caused by oleate in INS-1 cells

Laura Segall1, Nathalie Lameloise2, Françoise Assimacopoulos-Jeannet2, Enrique Roche1, Pamela Corkey3, Stéphane Thumelin1, Barbara E. Corkey3, and Marc Prentki1

1 Molecular Nutrition Unit, Department of Nutrition, University of Montreal, and the Centre de Recherche du Centre Hospitalier de l'Université de Montréal and Institut du Cancer, Montreal, Quebec, Canada H2L 4M1; 2 Department of Medical Biochemistry, Centre Médical Universitaire, University of Geneva, Geneva, Switzerland 1211; and 3 Center for Obesity and Metabolism at Boston University Medical Center, Boston University Medical School, Boston, Massachussets 02118

A comprehensive metabolic study was carried out to understand how chronic exposure of pancreatic beta -cells to fatty acids causes high basal secretion and impairs glucose-induced insulin release. INS-1 beta -cells were exposed to 0.4 mM oleate for 3 days and subsequently incubated at 5 or 25 mM glucose, after which various parameters were measured. Chronic oleate promoted triglyceride deposition, increased fatty acid oxidation and esterification, and reduced malonyl-CoA at low glucose in association with elevated basal O2 consumption and redox state. Oleate caused a modest (25%) reduction in glucose oxidation but did not affect glucose usage, the glucose 6-phosphate and citrate contents, and the activity of pyruvate dehydrogenase of INS-1 cells. Thus changes in glucose metabolism and a Randle-glucose/fatty acid cycle do not explain the altered secretory properties of beta -cells exposed to fatty acids. The main response of INS-1 cells to chronic oleate, which is to increase the oxidation and esterification of fatty acids, may contribute to cause high basal insulin secretion via increased production of reducing equivalents and/or the generation of complex lipid messenger molecule(s).

fatty acids; insulin secretion; obesity; type 2 diabetes


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