Adipose Tissue-Specific Deletion of 12-15-Lipoxygenase Protects Mice from the Consequences of a High-Fat DietReport as inadecuate




Adipose Tissue-Specific Deletion of 12-15-Lipoxygenase Protects Mice from the Consequences of a High-Fat Diet - Download this document for free, or read online. Document in PDF available to download.

Mediators of InflammationVolume 2012 2012, Article ID 851798, 13 pages

Research ArticleDepartment of Internal Medicine, Strelitz Diabetes Center, Eastern Virginia Medical School, Norfolk, VA 23507, USA

Received 23 September 2012; Accepted 28 November 2012

Academic Editor: Aldo Pende

Copyright © 2012 Banumathi K. Cole et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Type 2 diabetes is associated with obesity, insulin resistance, and inflammation in adipose tissue. 12-15-Lipoxygenase 12-15-LO generates proinflammatory lipid mediators, which induce inflammation in adipose tissue. Therefore we investigated the role of 12-15-LO activity in mouse white adipose tissue in promoting obesity-induced local and systemic inflammatory consequences. We generated a mouse model for fat-specific deletion of 12-15-LO, aP2-Cre; 12-15-LO

, which we call ad-12-15-LO mice, and placed wild-type controls and ad-12-15-LO mice on a high-fat diet for 16 weeks and examined obesity-induced inflammation and insulin resistance. High-fat diet-fed ad-12-15-LO exhibited improved fasting glucose levels and glucose metabolism, and epididymal adipose tissue from these mice exhibited reduced inflammation and macrophage infiltration compared to wild-type mice. Furthermore, fat-specific deletion of 12-15-LO led to decreased peripheral pancreatic islet inflammation with enlarged pancreatic islets when mice were fed the high-fat diet compared to wild-type mice. These results suggest an interesting crosstalk between 12-15-LO expression in adipose tissue and inflammation in pancreatic islets. Therefore, deletion of 12-15-LO in adipose tissue can offer local and systemic protection from obesity-induced consequences, and blocking 12-15-LO activity in adipose tissue may be a novel therapeutic target in the treatment of type 2 diabetes.





Author: Banumathi K. Cole, Margaret A. Morris, Wojciech J. Grzesik, Kendall A. Leone, and Jerry L. Nadler

Source: https://www.hindawi.com/



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