3273 KB53 KB200420252023Kozinc, KatjaMajdič, GregorŠtrbenc, Malanštevilka:2letnik:60str. 55-66DOI:10.26873/SVR-1519-2023ISSN:1580-4003COBISSID_HOST:161721347URN:URN:NBN:SI:doc-42GMDDHIenZaložba Univerze v LjubljaniSlovenian veterinary researchageautochthonous breedsFibroblast Growth FactorsGonadal HormoneshaematologyMicePlaque, AtheroscleroticPosavje horsesexFemale gonadal hormones are a risk factor for developing atherosclerotic changes in C57BL/6J mice on atherogenic diet|In humans, estrogens are considered protective factor against atherosclerosis because the risk increases in postmenopausal women. However, it is not clear whether estrogens are the only factor, whether sex chromosomes also have an influence, and whether estrogens play the same role in all mammals. The mouse line C57BL/6J is prone to develop atherosclerotic changes in the largest arteries after prolonged feeding of a high-fat diet containing cholesterol and cholate (Paigen diet). We aimed to examine effect of sex hormones and sex chromosome complement on the development of atherosclerotic plaques using agonadal SF-1 knockout mouse on C57BL/6J background. Gonadally intact and prepubertally gonadectomized WT and agonadal SF-1 knockout C57BL/6J mice of both sexes were exposed to a Paigen diet and a control diet for 20 weeks. We monitored their body weight, food intake, and serum lipid profile. The aortas were examined by the en face method, and the cross sections of the aortic bulbs were stained for lipid content. In all groups of mice, atherosclerotic changes were small and confined to the aortic bulb. The formation of atherosclerotic plaques was sex- and hormone-dependent, as female animals with functioning ovaries developed the most prominent atherosclerotic plaques. Gonadally intact females were also the only group that gained weight comparably on control or atherogenic diet. Diet affected blood biochemistry, but there were almost no significant differences between groups in serum lipid levels. Results indicated main mechanism causing sex-dependent differences in atherosclerosis depends on sex hormones rather than sex chromosomes. Our results also suggest that a mouse model of dietary induced atherosclerosis is of limited use to study the mechanisms of atherosclerosis in humans because the presence of estrogens impairs lipid metabolism and contributes to the formation of atherosclerotic plaquesTEXTznanstveno časopisjejournalsSlovenian National E-content AggregatorNational and University Library of SloveniaUniverza v Ljubljani, Veterinarska fakulteta