Diabetes promotes an inflammatory macrophage phenotype and atherosclerosis through acyl-CoA synthetase 1.

@article{Kanter2012DiabetesPA,
  title={Diabetes promotes an inflammatory macrophage phenotype and atherosclerosis through acyl-CoA synthetase 1.},
  author={Jenny E Kanter and Farah Kramer and Shelley Barnhart and Michelle M. Averill and Anuradha Vivekanandan-Giri and Thad Vickery and Lei Li and Lev Becker and Wei Yuan and Alan Chait and Kathleen R. Braun and Susan Potter-Perigo and Srinath Sanda and Thomas N Wight and Subramaniam Pennathur and Charles N Serhan and Jay W. Heinecke and Rosalind A Coleman and Karin E Bornfeldt},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2012},
  volume={109 12},
  pages={E715-24}
}
The mechanisms that promote an inflammatory environment and accelerated atherosclerosis in diabetes are poorly understood. We show that macrophages isolated from two different mouse models of type 1 diabetes exhibit an inflammatory phenotype. This inflammatory phenotype associates with increased expression of long-chain acyl-CoA synthetase 1 (ACSL1), an enzyme that catalyzes the thioesterification of fatty acids. Monocytes from humans and mice with type 1 diabetes also exhibit increased ACSL1… CONTINUE READING
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