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Biochem Biophys Res Commun. 2014 Aug 8;450(4):1619-25. doi: 10.1016/j.bbrc.2014.07.048. Epub 2014 Jul 15.

PKCδ regulates hepatic triglyceride accumulation and insulin signaling in Lepr(db/db) mice.

Author information

1
Boshell Diabetes and Metabolic Disease Research Program, Auburn University, Auburn, AL 36849, United States; College of Human Sciences, Auburn University, Auburn, AL 36849, United States.
2
Bassett Research Institute, Bassett Medical Center, Bassett Healthcare Network, Cooperstown, NY 13326, United States.
3
Department of Pathology, Bassett Medical Center, Bassett Healthcare Network, Cooperstown, NY 13326, United States.
4
Department of Internal Medicine, Bassett Medical Center, Bassett Healthcare Network, Cooperstown, NY 13326, United States.
5
Boshell Diabetes and Metabolic Disease Research Program, Auburn University, Auburn, AL 36849, United States; College of Human Sciences, Auburn University, Auburn, AL 36849, United States; Bassett Research Institute, Bassett Medical Center, Bassett Healthcare Network, Cooperstown, NY 13326, United States. Electronic address: mwgreene@auburn.edu.

Abstract

PKCδ has been linked to key pathophysiological features of non-alcoholic fatty liver disease (NAFLD). Yet, our knowledge of PKCδ's role in NAFLD development and progression in obese models is limited. PKCδ(-/-)/Lepr(db)(/)(db) mice were generated to evaluate key pathophysiological features of NAFLD in mice. Hepatic histology, oxidative stress, apoptosis, gene expression, insulin signaling, and serum parameters were analyzed in Lepr(db)(/)(db) and PKCδ(-/-)/Lepr(db)(/)(db) mice. The absence of PKCδ did not abrogate the development of obesity in Lepr(db)(/)(db) mice. In contrast, serum triglyceride levels and epididymal white adipose tissue weight normalized to body weight were reduced in PKCδ(-/-)/Lepr(db)(/)(db) mice compared Lepr(db)(/)(db) mice. Analysis of insulin signaling in mice revealed that hepatic Akt and GSK3β phosphorylation were strongly stimulated by insulin in PKCδ(-/-)/Lepr(db)(/)(db) compared Lepr(db)(/)(db) mice. PKCδ may be involved in the development of obesity-associated NAFLD by regulating hepatic lipid metabolism and insulin signaling.

KEYWORDS:

Insulin resistance; Obesity; Oxidative stress; Steatosis

PMID:
25035929
DOI:
10.1016/j.bbrc.2014.07.048
[Indexed for MEDLINE]

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