Journal
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 470, Issue 2, Pages 153-162Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2007.11.017
Keywords
pancreatic islets; INS-1 832/13 cells; anaplerosis; acetyl-CoA carboxylase; fatty acid synthase; cholesterol esters; phospholipids; lipogenesis; lipid remodeling
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Funding
- NIDDK NIH HHS [DK28348, R01 DK028348-24, R01 DK028348] Funding Source: Medline
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Pancreatic beta cell mitochondria convert insulin secretagogues into products that support insulin exocytosis. We explored the idea that lipids are some of these products formed from acyl group transfer out of mitochondria to the cytosol, the site of lipid synthesis. There are two isoforms of acetyl-CoA carboxylase, the enzyme that forms malonyl-CoA from which C-2 units for lipid synthesis are formed. We found that ACC1, the isoform seen in lipogenic tissues, is the only isoform present in human and rat pancreatic islets and INS-1 832/13 cells. Inhibitors of ACC and fatty acid synthase inhibited insulin release in islets and INS-1 cells. Carbon from glucose and pyruvate were rapidly incorporated into many lipid classes in INS-1 cells. Glucose and other insulin secretagogues acutely increased many lipids with C-14-C-24 chains including individual cholesterol esters, phospholipids and fatty acids. Many phosphatidylcholines and phosphatidylserines were increased and many phosphatidylinositols and several phosphatidylethanolamines were decreased. The results suggest that lipid remodeling and rapid lipogenesis from secretagogue carbon support insulin secretion. (c) 2007 Elsevier Inc. All rights reserved.
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