Nonobese Diabetic (NOD) Mice Congenic for a Targeted Deletion of 12/15-Lipoxygenase Are Protected From Autoimmune Diabetes
Author(s) -
Marcia McDuffie,
Nelly A. Maybee,
Susanna R. Keller,
Brian K. Stevens,
James C. Garmey,
Margaret Morris,
Elizabeth Kropf,
Claudia Rival,
Kaiwen Ma,
Jeffrey D. Carter,
Sarah A. Tersey,
Craig S. Nunemaker,
Jerry L. Nadler
Publication year - 2007
Publication title -
diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.219
H-Index - 330
eISSN - 1939-327X
pISSN - 0012-1797
DOI - 10.2337/db07-0830
Subject(s) - congenic , nod , autoimmune diabetes , nod mice , diabetes mellitus , immunology , autoimmunity , medicine , lipoxygenase , autoimmune disease , endocrinology , biology , type 1 diabetes , antibody , enzyme , genetics , biochemistry , gene
12/15-lipoxygenase (12/15-LO), one of a family of fatty acid oxidoreductase enzymes, reacts with polyenoic fatty acids to produce proinflammatory lipids. 12/15-LO is expressed in macrophages and pancreatic beta-cells. It enhances interleukin 12 production by macrophages, and several of its products induce apoptosis of beta-cells at nanomolar concentrations in vitro. We had previously demonstrated a role for 12/15-LO in beta-cell damage in the streptozotocin model of diabetes. Since the gene encoding 12/15-LO (gene designation Alox15) lies within the Idd4 diabetes susceptibility interval in NOD mice, we hypothesized that 12/15-LO is also a key regulator of diabetes susceptibility in the NOD mouse.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom