Journal
CELL METABOLISM
Volume 15, Issue 5, Pages 574-584Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2012.03.005
Keywords
-
Categories
Funding
- United States Public Health Service [DK-40936, DK-49230, DK-085638, DK-059635, DK-45735]
- Swiss National Science Foundation/Swiss Foundation for Grants in Biology and Medicine [PASMP3_132563]
- Swiss National Science Foundation (SNF) [PASMP3_132563] Funding Source: Swiss National Science Foundation (SNF)
Ask authors/readers for more resources
Nonalcoholic fatty liver disease (NAFLD) is now the most frequent chronic liver disease in Western societies, affecting one in four adults in the USA, and is strongly associated with hepatic insulin resistance, a major risk factor in the pathogenesis of type 2 diabetes. Although the cellular mechanisms underlying this relationship are unknown, hepatic accumulation of diacylglycerol (DAG) in both animals and humans has been linked to hepatic insulin resistance. In this Perspective, we discuss the role of DAG activation of protein kinase C epsilon as the mechanism responsible for NAFLD-associated hepatic insulin resistance seen in obesity, type 2 diabetes, and lipodystrophy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available