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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:991.)
© 2001 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

High-Fat, High-Cholesterol Diet Increases the Incidence of Gastritis in LDL Receptor–Negative Mice

Aino Laurila¹; Sheri P. Cole¹; Shiva Merat; Marygorret Obonyo; Wulf Palinski; Joshua Fierer; Joseph L. Witztum

From the Division of Endocrinology and Metabolism (A.L., S.M., W.P., J.L.W.) and Division of Infectious Diseases (S.P.C., M.O., J.F.), Department of Medicine, University of California, San Diego, and VA Healthcare San Diego (J.F.), La Jolla, Calif. The first 2 authors contributed equally to this work.

Correspondence to Joseph L. Witztum, MD, University of California, San Diego, 1080 Basic Science Bldg, 9500 Gilman Dr, La Jolla, CA 92093-0682. E-mail witztum{at}ucsd.edu

Abstract—Transgenic and knockout mice are widely used as models for atherogenesis studies. While developing a Helicobacter infection model in LDL receptor–negative (LDLR^-/-) mice, we noticed that mice fed a high-fat, high-cholesterol diet often contracted gastritis independent of infection. To further investigate this finding, we studied 27 male and 18 female LDLR^-/- mice fed high-fat, 1% or 1.25% cholesterol diets for 3 to 4 months. The extent of atherosclerosis was morphometrically analyzed in the whole aorta, and the degree of gastric inflammation was scored histologically in hematoxylin-eosin–stained stomach sections. The autoantibody titers to epitopes of oxidized LDL were also measured. Mice fed high-fat, high-cholesterol diets had a significantly higher incidence of gastritis than mice fed normal chow, 62% versus 5%, respectively (P<0.0001). This effect was specific for LDLR^-/- mice, because no difference in gastritis was found in wild-type mice fed either diet. Animals with gastritis showed slightly more atherosclerosis than animals without gastritis: 16.3±6.4% versus 12.8±3.4% in males and 9.4±3.5% versus 6.5±3.3% in females. Cholesterol-fed mice also had significantly higher IgG autoantibody titers against modified LDL than normal chow–fed animals, but no difference was seen between the gastritis and nongastritis groups. We conclude that the standard high-fat, high-cholesterol diet commonly used in many murine models to induce atherosclerosis increased the incidence of gastritis significantly in LDLR^-/- mice.

Key Words: inflammation • atherosclerosis • gastritis

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