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Deconstructing the Role of PKC Epsilon in Glucose Homeostasis


The failure of insulin to suppress glucose production by the liver is a key aspect of the insulin resistance seen in type 2 diabetes. Lipid-activated protein kinase C epsilon has long been identified as an important mediator of diet-induced glucose intolerance and hepatic insulin resistance and the current view emphasizes a mechanism involving phosphorylation of the insulin receptor by the kinase to inhibit downstream insulin action. However, the significance of this direct effect in the liver has now been challenged by tissue-specific deletion of PKCepsilon, which demonstrated a more prominent role for the kinase in adipose tissue to promote glucose intolerance. New insights regarding the role of PKCepsilon therefore contribute to the understanding of indirect effects on hepatic glucose metabolism.

Type Journal
ISBN 1879-3061 (Electronic) 1043-2760 (Linking)
Authors Schmitz-Peiffer, C.
Responsible Garvan Author A/Prof Carsten Schmitz-Peiffer
Published Date 2020-05-01
Published Volume 31
Published Issue 5
Published Pages 344-356
Status Published in-print
DOI 10.1016/j.tem.2020.01.016
URL link to publisher's version