Adipose Tissue-Specific Deletion of 12/15-Lipoxygenase Protects Mice from the Consequences of a High-Fat Diet
Hindawi Publishing Corporation
Mediators of Inflammation
Volume 2012, Article ID 851798, 13 pages doi:10.1155/2012/851798 Research Article
Adipose Tissue-Specific Deletion of 12/15-Lipoxygenase
Protects Mice from the Consequences of a High-Fat Diet
Banumathi K. Cole, Margaret A. Morris, Wojciech J. Grzesik,
Kendall A. Leone, and Jerry L. Nadler
Department of Internal Medicine, Strelitz Diabetes Center, Eastern Virginia Medical School, Norfolk, VA 23507, USA
Correspondence should be addressed to Banumathi K. Cole, colebk@evms.edu and Jerry L. Nadler, nadlerjl@evms.edu
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. 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-LOloxP/loxP , 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
Mediators of Inflammation
Volume 2012, Article ID 851798, 13 pages doi:10.1155/2012/851798 Research Article
Adipose Tissue-Specific Deletion of 12/15-Lipoxygenase
Protects Mice from the Consequences of a High-Fat Diet
Banumathi K. Cole, Margaret A. Morris, Wojciech J. Grzesik,
Kendall A. Leone, and Jerry L. Nadler
Department of Internal Medicine, Strelitz Diabetes Center, Eastern Virginia Medical School, Norfolk, VA 23507, USA
Correspondence should be addressed to Banumathi K. Cole, colebk@evms.edu and Jerry L. Nadler, nadlerjl@evms.edu
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. 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-LOloxP/loxP , 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
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