Metabolic Role of PTEN in Insulin Signaling and Resistance
- 1Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario M5G 2C4, Canada
- 2Institute of Medical Science, University of Toronto, Toronto, Ontario M5G 2M9, Canada
- 3Department of Developmental and Molecular Biology and Medicine (Oncology), Albert Einstein College of Medicine and Albert Einstein Cancer Center, Bronx, New York 10461, USA
- 4Department of Immunology, University of Toronto, Toronto, Ontario M5G 2M9, Canada
- 5Division of Endocrinology and Metabolism, Department of Medicine, University Health Network/Mount Sinai Hospital, University of Toronto, Toronto, Ontario M5G 2C4, Canada
- Correspondence: mwoo{at}uhnresearch.ca; antonio.dicristofano{at}einstein.yu.edu
Abstract
Phosphatase and tensin homolog (PTEN) is most prominently known for its function in tumorigenesis. However, a metabolic role of PTEN is emerging as a result of its altered expression in type 2 diabetes (T2D), which results in impaired insulin signaling and promotion of insulin resistance during the pathogenesis of T2D. PTEN functions in regulating insulin signaling across different organs have been identified. Through the use of a variety of models, such as tissue-specific knockout (KO) mice and in vitro cell cultures, PTEN's role in regulating insulin action has been elucidated across many cell types. Herein, we will review the recent advancements in the understanding of PTEN's metabolic functions in each of the tissues and cell types that contribute to regulating systemic insulin sensitivity and discuss how PTEN may represent a promising therapeutic strategy for treatment or prevention of T2D.
