ArticleAnimal models and experimental medicine2026
A high-fat diet with vitamin D and propylthiouracil produces a pro-atherogenic phenotype in rats.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtherosclerosis begins with dyslipidemia, vascular inflammation, and endothelial dysfunction. Rodent models that capture these early events are needed for mechanistic and interventional studies. This study evaluated whether a cholesterol-rich, high-fat diet (HFD) supplemented with vitamin D and propylthiouracil (PTU) promotes a pro-atherogenic phenotype in rats, as evidenced by dyslipidemia, inflammation, markers of endothelial dysfunction, and early vascular remodeling.
methodsMale Sprague-Dawley rats (n = 18) received standard chow or a HFD containing 2% cholesterol, 3% lard, 0.5% cholate, vitamin D (200 000 IU/kg), and PTU (0.2% w/w) for 11 weeks. Terminal serum total cholesterol, high-density lipoprotein, low-density lipoprotein (LDL)/very low-density lipoprotein (VLDL), triglycerides, calcium, interleukin-6 (IL-6), C-reactive protein, serum amyloid A (SAA), circulating endothelial nitric oxide synthase (eNOS), and intracellular adhesion molecule-1 (ICAM-1) were measured. The aorta, the coronary arteries, and the liver were examined histologically.
resultsHFD-fed rats developed significant hypercholesterolemia with higher total cholesterol and LDL/VLDL (p < 0.0001) and lower triglycerides (p < 0.0001) versus controls. Serum calcium was higher (p < 0.0001) without vascular calcification. Aortae exhibited wall thickening, smooth-muscle disarray, mononuclear infiltrates, and focal foam cell-like changes; coronary arteries exhibited endothelial irregularities and perivascular infiltrates. Livers exhibited micro- and macrovesicular steatosis. IL-6 and SAA were higher (p < 0.05), and circulating eNOS was lower (p < 0.05); ICAM-1 did not differ significantly.
conclusionAn 11-week vitamin D/PTU-supplemented HFD induces an LDL-dominant dyslipidemia with systemic inflammation and evidence consistent with endothelial dysfunction, alongside histological features of early vascular remodeling and hepatic steatosis. This nongenetic model may be useful for studying early atherogenic changes.
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