Journal
CELL
Volume 148, Issue 5, Pages 852-871Publisher
CELL PRESS
DOI: 10.1016/j.cell.2012.02.017
Keywords
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Funding
- Howard Hughes Medical Institute
- Veterans Affairs Merit Review Program
- United States Department of Health and Human Services [DK-40936, DK-49230, DK-059635, DK-45735, DK-08638]
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Insulin resistance is a complex metabolic disorder that defies explanation by a single etiological pathway. Accumulation of ectopic lipid metabolites, activation of the unfolded protein response (UPR) pathway, and innate immune pathways have all been implicated in the pathogenesis of insulin resistance. However, these pathways are also closely linked to changes in fatty acid uptake, lipogenesis, and energy expenditure that can impact ectopic lipid deposition. Ultimately, these cellular changes may converge to promote the accumulation of specific lipid metabolites (diacylglycerols and/or ceramides) in liver and skeletal muscle, a common final pathway leading to impaired insulin signaling and insulin resistance.
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