Effects of dietary fats from animal and plant sources on diet-induced fatty streak lesions in C57BL/6J mice.
نویسندگان
چکیده
This study was designed to determine the effects of a variety of naturally occurring saturated fats on aortic lesion formation in C57BL/6J mice that are susceptible to diet-induced fatty streak lesions. Groups of female mice were randomly assigned to one of seven treatment groups and were fed diets containing 15% (w/w) hydrogenated coconut oil, hydrogenated soy oil, hydrogenated palm oil, cocoa butter, lard, tallow, or dairy butter, 1% cholesterol, and 0.5% cholic acid. Plasma lipid levels were measured to determine whether lesion formation was related to specific changes in these parameters. Lesions, which were observed in all groups of mice, ranged from 420 to 3220 microns2/aortic cross section. Lesion area was positively correlated to the percentage of saturated fatty acids contained in the fat sources and the ratio of combined VLDL plus LDL-cholesterol to HDL-cholesterol and inversely correlated to monounsaturated fatty acids content and to HDL-cholesterol levels. Results from this study demonstrate that inbred mice may provide a good model for dissecting the genetic basis for the differential atherogenic responses to diet-induction and for studying the effects of dietary factors on aortic lesion development.
منابع مشابه
Genetic-dietary regulation of serum paraoxonase expression and its role in atherogenesis in a mouse model.
In an effort to identify genetic factors contributing to atherogenesis, we have studied inbred strains of mice that are susceptible (C57BL/6J) and resistant (C3H/HeJ) to diet-induced aortic fatty streak lesions. When maintained on a low-fat diet, HDL isolated from both strain C57BL/6J (B6) and C3H/HeJ (C3H) mice protect against LDL oxidation in a coculture model of the artery wall. However, whe...
متن کامل3-deazaadenosine prevents adhesion molecule expression and atherosclerotic lesion formation in the aortas of C57BL/6J mice.
Adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) play an important role during the development of atherosclerosis. 3-Deazaadenosine (c(3)Ado), an adenosine analogue, inhibits endothelial-leukocyte adhesion and ICAM-1-expression in vitro. We hypothesized that c(3)Ado is able to prevent the expression of adhesion molecules and at...
متن کاملFormation in the Aortas of C57BL/6J Mice 3-Deazaadenosine Prevents Adhesion Molecule Expression and Atherosclerotic Lesion
Adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) play an important role during the development of atherosclerosis. 3-Deazaadenosine (cAdo), an adenosine analogue, inhibits endothelial-leukocyte adhesion and ICAM-1-expression in vitro. We hypothesized that cAdo is able to prevent the expression of adhesion molecules and atherosc...
متن کاملDietary antioxidants do not reduce fatty streak formation in the C57BL/6 mouse atherosclerosis model.
Epidemiological studies and animal trials have suggested that dietary antioxidants protect against atherosclerosis. To test this hypothesis, C57BL/6 mice were fed atherogenic diets supplemented with either vitamin E or butylated hydroxytoluene (BHT). Three groups of 20 mice were fed for 15 weeks on diets containing 1% cholesterol and 0.5% cholic acid. The diet of two groups was supplemented wit...
متن کاملImidacloprid Promotes High Fat Diet-Induced Adiposity and Insulin Resistance in Male C57BL/6J Mice
Imidacloprid, a neonicotinoid insecticide widely used in agriculture worldwide, has been reported to promote adipogenesis and cause insulin resistance in vitro. The purpose of the current study was to determine the effects of imidacloprid and its interaction with dietary fat in the development of adiposity and insulin resistance using male C57BL/6J mice. Imidacloprid (0.06, 0.6, or 6 mg/kg bw/d...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Journal of lipid research
دوره 34 8 شماره
صفحات -
تاریخ انتشار 1993