Back to Journals » Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy » Volume 7

Linking obesity with type 2 diabetes: the role of T-bet

Authors Wali J, Thomas H, Sutherland APR

Received 3 March 2014

Accepted for publication 29 April 2014

Published 22 July 2014 Volume 2014:7 Pages 331—340

DOI https://doi.org/10.2147/DMSO.S51432

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4


Jibran A Wali,1,2 Helen E Thomas,1,2 Andrew PR Sutherland1

1Immunology and Diabetes Unit, St Vincent's Institute, 2Department of Medicine, St Vincent's Hospital, University of Melbourne, Fitzroy, Victoria, Australia

Abstract: Obesity is a major predisposing factor for the development of type 2 diabetes (T2D) and is an escalating public health issue around the world. The transition from obesity to T2D is preceded by the induction of a state of insulin resistance, which occurs in response to genetic factors and environmental influences, such as diet. Recent advances have implicated inflammatory immune cells and cytokines as critical pathogenic mediators of insulin resistance and T2D. In particular proinflammatory T helper (Th)1 cells and M1 macrophages are recruited to adipose tissue in response to high fat diet and directly promote the development of insulin resistance. The function of these two cell types is linked by the actions of the cytokine interferon (IFN)γ and one of its major transcriptional regulators T-bet. Recent studies in animal models of T2D demonstrate that T-bet is critical for the development of insulin resistance in response to high fat diet as T-bet-deficient animals are protected from the development of insulin resistance. These data indicate that T-bet and type 1 immunity may constitute novel sites of therapeutic intervention for the treatment of insulin resistance and T2D, in obese human patients.

Keywords: type 2 diabetes, obesity, insulin resistance, immune system, T-bet, Th1, IFNγ

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]