Atypical xanthomatosis in apolipoprotein E-deficient mice after cholesterol feeding
article
Apolipoprotein (apo) E-deficient mice were fed a hypercholesterolemic diet for 14 weeks. Mean serum cholesterol levels rose to 37.5 mM. Upon complete necroscopy, massive xanthomatous lesions were noticed in various tissues, with a predilection for subcutaneous and peritendinous tissues, while control animals on the same diet (3.4 mM serum cholesterol) and apo E-deficient mice on a regular chow diet (20 mM serum cholesterol) did not show such lesions. Also, apo E3-Leiden transgenic mice fed a high fat diet, with 60 mM of serum cholesterol, did not exhibit any xanthomatosis. The xanthomatous lesions found in the Apoe knock-out mouse clearly differed in location from xanthomas previously found in low density lipoprotein receptor-deficient mice. We conclude that the lack of apo E results in atypical disseminated xanthomatosis, suggesting that apo E has an important role in determining the tissue distribution of cholesterol deposition. Chemicals/CAS: cholesterol, 57-88-5; Apolipoproteins E; Cholesterol, Dietary
Topics
Cholesterol depositionFamilial dysbetalipoproteinemiaGene targetingHypercholesterolemiaLipoprotein metabolismMouse modelapolipoprotein echolesterolanimal experimentanimal modelarticlecholesterol dietfamilial hypercholesterolemiagene targetinghistologyhyperlipoproteinemia type 3lipoprotein metabolismmousenonhumanpriority journalxanthomatosisAnimalApolipoproteins ECholesterol, DietaryHumanMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicSupport, Non-U.S. Gov'tXanthomatosis
TNO Identifier
232813
ISSN
00219150
Source
Atherosclerosis, 112(2), pp. 237-243.
Pages
237-243
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