Aberrant lipid metabolism disrupts calcium homeostasis causing liver endoplasmic reticulum stress in obesity

Suneng Fu, Ling Yang, Ping Li, Oliver Hofmann, Lee Dicker, Winston Hide, Xihong Lin, Steven M. Watkins, Alexander R. Ivanov and Gökhan S. Hotamisligil ()
Additional contact information
Suneng Fu: and Nutrition, Harvard School of Public Health
Ling Yang: and Nutrition, Harvard School of Public Health
Ping Li: and Nutrition, Harvard School of Public Health
Oliver Hofmann: Harvard School of Public Health
Lee Dicker: Harvard School of Public Health
Winston Hide: Harvard School of Public Health
Xihong Lin: Harvard School of Public Health
Steven M. Watkins: Lipomics Technologies Inc
Alexander R. Ivanov: and Nutrition, Harvard School of Public Health
Gökhan S. Hotamisligil: and Nutrition, Harvard School of Public Health

Nature, 2011, vol. 473, issue 7348, 528-531

Abstract: Lipid metabolism in obesity The function of the endoplasmic reticulum (ER) changes during obesity: in the liver, ER-associated protein synthesis slows down, and genes involved in lipid metabolism are switched on. ER stress is an important factor in obesity, insulin resistance and type 2 diabetes. A possible mechanism for this link has now been identified. Perturbation of fatty acid and lipid metabolism in the ER inhibits the activity of SERCA, the main ER calcium importer. Changing the lipid composition or increasing the amount of SERCA in the ER is shown to relieve the stress and improve glucose homeostasis in vivo.

Date: 2011
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DOI: 10.1038/nature09968

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