harlan teklad官网代理商 动物饲料 动脉粥样硬化 胆固醇和胆酸 TD.88051

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harlan teklad官网代理商 动物饲料 动脉粥样硬化 胆固醇和胆酸 TD.88051

harlan teklad官网代理商 动物饲料

动脉粥样硬化

在实验动物模型中，饮食是诱导或加速动脉粥样硬化的有用工具。用于诱发啮齿类动物动脉粥样硬化的主要饮食特征因研究模型、所需终点和喂养时间的不同而不同。尽管动脉粥样硬化饮食的配方在不断发展，但文献中详细描述的备选方案概述如下。有关每个饮食选项和文献参考的更多信息，请参见节目表后面的可扩展选项卡。

研究用途 主要饮食特征 实例
“西方”纯正致动脉粥样硬化饮食
加速高胆固醇血症和斑块形成的转基因模型，如APOE和Ldlr缺乏的小鼠。用于饮食诱导肥胖的各种啮齿动物模型。
  • 高脂饮食(按体重计算占20-23%；脂肪占40-45%)
  • 饱和脂肪酸(SFA>总脂肪酸的60%)
  • 乳脂/乳脂
  • 蔗糖(按重量计占34%)
  • 胆固醇(总数0.2%)
 TD.88137
TD.10885
添加胆固醇和胆酸来源的“西方”纯动脉粥样硬化饮食*
在野生型小鼠和大鼠中诱导高胆固醇血症和轻度动脉粥样硬化(泡沫细胞、脂肪条纹)。不会助长肥胖。
  • 高脂饮食(体重15-20%；脂肪34-45千卡)
  • 饱和脂肪酸(SFA>总脂肪酸的55%)
  • 乳脂/黄油、可可脂
  • 蔗糖(重量占30%-50%)
  • 胆固醇(1-1.25%)
  • 巧克力来源(0.5%)*
 TD.02028
TD.09237
添加胆固醇和胆酸盐的混合高脂饮食*
在野生型小鼠和大鼠中诱导高胆固醇血症和轻度动脉粥样硬化(泡沫细胞、脂肪条纹)。不会助长肥胖。
也用于造石(胆石)啮齿动物的研究。
  • 75%的啮齿动物饲养员；25%的纯化成分
  • 高脂肪(体重约15%；脂肪37%千卡)
  • 饱和脂肪酸(SFA>总脂肪酸的45%)
  • 胆固醇(1.25%)
  • 巧克力源(0.5%)*
 TD.88051
TD.90221
添加胆固醇的标准饮食
在转基因和野生型模型中诱导高胆固醇血症而不促进肥胖。
  • 标准的、以谷物为基础的啮齿动物饮食
  • 最小/中度植物雌激素饮食建议
  • 胆固醇(1-4%)
 TD.120097
TD.07841
TD.01383

*胆酸钠或胆酸有助胆固醇和脂肪的吸收，并可透过胆汁酸合成减少胆固醇的排出。然而，如果你的研究不想包括胆酸盐的来源，没有胆酸盐的饮食是可用的。

折叠所有标签

“西式”饮食被喂给基因修饰的心血管模型，如APOE和Ldlr缺乏的小鼠，以加速和促进高胆固醇血症和斑块形成，并引出通常与代谢综合征相关的表型。在动脉粥样硬化的文献中，“西方”饮食通常被描述为含有20-23%乳脂/蝴蝶脂肪、0.2%总胆固醇和34%蔗糖的纯啮齿动物饮食。TD.88137这是一种“西式”饮食的例子，最初的目的是在一种新生成的APOE缺陷小鼠模型中描述和促进动脉粥样硬化的发展。联系我们，以获得更多关于“西方”风格的饮食，修改，或可能的控制饮食。
例子：

  • TD.88137调整卡路里饮食(42%来自脂肪，0.2%总胆固醇)
  • TD.1088545%脂肪KCAL饮食(总胆固醇0.2%)

研究用途：
加速高胆固醇血症和斑块形成的转基因模型，如APOE和Ldlr缺乏的小鼠。
用于饮食诱导肥胖的各种啮齿动物模型。
主要饮食特征：

  • 高脂肪饮食(按体重计算占20-23%；脂肪占40-45%)
  • 饱和脂肪酸(SFA>总脂肪酸的60%)
  • 乳脂/乳脂
  • 蔗糖(按重量计占34%)
  • 胆固醇(总数0.2%)

参考资料：

  1. Febbraio，M，等人，B类清道夫受体CD 36的靶向性破坏对小鼠动脉粥样硬化病变的发展有保护作用。j Clin Investment，2000年。105(8)：P。1049-56
  2. Huszar，D，等人，在低密度脂蛋白受体缺乏的小鼠体内增加了低密度脂蛋白胆固醇和动脉粥样硬化，减少了清道夫受体B1的表达。Arteroscler Thromb VASc Biol，2000年。20(4)：P。1068-73
  3. Nakashima，Y.，等人，ApoE缺乏的小鼠在整个动脉树形成动脉粥样硬化的各个阶段的病变。Arteroscler Thromb，1994年。14(1)：P。133-40
  4. 中岛，Y，等，VCAM-1和ICAM-1在ApoE缺乏的小鼠内皮动脉粥样硬化易发部位上调VCAM-1和ICAM-1的表达。Arteroscler Thromb VASc Biol，1998年。18(5)：P。842-51
  5. Plump，A.S.等人，ES细胞同源重组所致载脂蛋白E缺陷小鼠的严重高胆固醇血症和动脉粥样硬化。细胞，1992年。71(2)：P。343-53
  6. Towler，D.A.等，饮食诱导的糖尿病激活了低密度脂蛋白受体缺陷小鼠主动脉的成骨基因调控程序。j Biol Chem，1998年。273(46)：P。30427-34。
  7. Foxos整合胰岛素在血管内皮细胞中的多向性作用，以保护小鼠免受动脉粥样硬化的影响。Metab细胞，2012年。15(3)：P。372-81。
野生型小鼠和大鼠一般对动脉粥样硬化有抵抗力，需要更极端的饮食操作来改变脂蛋白谱，形成轻度动脉粥样硬化(泡沫细胞、脂肪条纹)。现代配方完全是由纯化成分制成的，因为据报道，这种更精细的方法可以减少较少精制和较传统饮食方法引起的胆结石和肝脏损害的发生率。为了在野生型动物中诱导轻度动脉粥样硬化，可对“西方”纯化饲料进行改良，以提高胆固醇(1-1.25%)，并添加胆酸钠或胆酸等胆盐。联系我们获得更多的信息，修改，或可能的控制饮食。
添加胆固醇和胆酸盐来源的纯化高脂饮食的例子*：

  • TD.0202821%乳脂(1.25%胆固醇，0.5%胆酸)
  • TD.0923715%乳脂饮食(1%胆固醇，0.5%胆酸钠)

添加胆固醇的纯化高脂饮食的例子(没有胆酸来源)：

  • TD.9612121%乳脂(1.25%胆固醇)

研究用途：
主要在野生型小鼠和大鼠诱发高胆固醇血症和轻度动脉粥样硬化(泡沫细胞、脂肪条纹)。
不会助长肥胖。
主要饮食特征：

  • 高脂饮食(体重15-20%；脂肪34-45千卡)
  • 饱和脂肪酸(SFA>总脂肪酸的55%)
  • 乳脂/黄油、可可脂
  • 蔗糖(重量占30%-50%)
  • 胆固醇(1-1.25%)
  • 巧克力源(0.5%)*

参考资料：

  1. 番茄汁番茄红素对大鼠肝脏脂肪变性的影响。j Nutr Biochem，2013年。24(11)：P。1870-81
  2. 高，Q，等，动脉粥样硬化饮食加剧了小鼠缺乏谷胱甘肽过氧化物酶结肠炎。炎症肠Dis，2010年。16(12)：P。2043-54
  3. Lichtman，A.H.，等，高脂血症和动脉粥样硬化病变的发展，低密度脂蛋白受体缺乏的小鼠，喂食定义半纯化饮食与不含胆酸。Arteroscler Thromb VASc Biol，1999年。19(8)：P。1938-44年。
  4. 慢性精神应激和致动脉粥样硬化饮食对小鼠主动脉免疫炎症环境的影响。BrainBehav Immun，2011年。25(8)：P。1649-57
  5. Nishina，P.m.，等，动物和植物来源的饮食脂肪对C57BL/6J小鼠因饮食引起的脂肪条纹损害的影响。j Lipid RES，1993年。34(8)：P。1413-22
  6. Nishina，P.m.，等，9种近交系小鼠动脉粥样硬化及血浆和肝脏脂质。脂质，1993年。28(7)：P。599-605
  7. 月，P，等，增强CD 36空小鼠肝脏载脂蛋白A-I分泌及胆固醇和磷脂的外周流出。PLOS One，2010年。5(3)：P。E 9906
  8. Nishina，下午，J.Verstuyft，B.Paigen，合成低脂和高脂肪饮食，用于研究小鼠动脉粥样硬化。j Lipid RES，1990年。31(5)：P。859-69

*胆酸钠或胆酸有助胆固醇和脂肪的吸收，并可透过胆汁酸合成减少胆固醇的排出。然而，如果你的研究不想包括胆酸盐的来源，没有胆酸盐的饮食是可用的。看见TD.96121为了纯正的饮食TD.94059混合饮食。请与我们联系，了解其他选项。

贝弗利·派根和他的同事首先通过喂养一种混合性动脉粥样硬化饮食来描述C57BL/6小鼠动脉粥样硬化的发展。这种混合饲料是通过将一种天然成分的老鼠饲料按3：1的比例与浓缩的纯化饲料(含5%胆固醇和2%胆酸钠；称为Thoms-Hartroft饮食)混合而成的。产生的混合物在TD.88051/TD.90221(同配方)含有~15.8%脂肪、1.25%胆固醇和0.5%胆酸钠。这组人后来将混合动脉粥样硬化饮食方法与更现代的“西方”纯化动脉粥样硬化饮食方法进行了比较，并添加了胆固醇和胆酸盐，发现混合动脉粥样硬化饮食会导致更多的胆结石和肝脏损伤。混合饮食含有多种未精制的成分，这些成分可能会改变血脂代谢和动脉粥样硬化的发生，并且不允许对成分和营养物进行精确控制，以用于慢性病的研究。虽然已经开发出了更精细的饮食，但混合动脉粥样硬化饮食仍然是野生型小鼠和大鼠诱发轻度动脉粥样硬化和胆结石的流行食品。联系我们获得更多的信息，修改，或可能的控制饮食。
添加胆固醇和胆酸盐的混合高脂饮食实例*：

  • TD.88051和TD.90221(相同的配方)是特克拉德混合动脉粥样硬化饮食的产品代码。

添加胆固醇的混合高脂饮食的例子(没有胆酸来源)：

  • TD.94059

研究用途：
主要在野生型小鼠和大鼠诱发高胆固醇血症和轻度动脉粥样硬化(泡沫细胞、脂肪条纹)。
不会助长肥胖。
也用于造石(胆石)啮齿动物的研究。
主要饮食特征：

  • 75%的啮齿动物饲养员；25%的纯化成分
  • 高脂肪(体重约15%；脂肪37%千卡)
  • 饱和脂肪酸(SFA>总脂肪酸的45%)
  • 胆固醇(1.25%)
  • 巧克力源(0.5%)*

参考资料：

  1. Nishina，下午，J.Verstuyft，B.Paigen，合成低脂和高脂肪饮食，用于研究小鼠动脉粥样硬化。j Lipid RES，1990年。31(5)：P。859-69
  2. Clee，S.M.，等，血浆和血管壁脂蛋白脂肪酶在动脉粥样硬化中有不同的作用。j Lipid RES，2000年。41(4)：P。521-31
  3. George，J.等人，用热休克蛋白-65免疫C57BL/6J小鼠，促进了脂肪条纹的形成。Arteroscler Thromb VASc Biol，1999年。19(3)：P。505-10
  4. Miyake，J.H.，等，胆固醇-7-α-羟化酶基因表达对C57BL/6J小鼠动脉粥样硬化的预防作用。Arteroscler Thromb VASc Biol，2002年。22(1)：P。121-6
  5. Paigen，B，等，小鼠动脉粥样硬化病变的定量评估。动脉粥样硬化，1987年。68(3)：P。231-40。
  6. Schreyer，S.A.，D.L.Wilson和R.C.LeBoeuf，C57BL/6小鼠以高脂饮食作为糖尿病加速动脉粥样硬化的模型。动脉粥样硬化，1998年。136(1)：P。17-24。
  7. Vergnes，L，等，胆固醇和胆酸组成的动脉粥样硬化饮食诱导不同阶段的肝脏炎症基因的表达。j Biol Chem，2003年。278(44)：P。42774-84。

*胆酸钠或胆酸有助胆固醇和脂肪的吸收，并可透过胆汁酸合成减少胆固醇的排出。然而，如果你的研究不想包括胆酸盐的来源，没有胆酸盐的饮食是可用的。看见TD.96121为了纯正的饮食TD.94059混合饮食。请与我们联系，了解其他选项。

标准的，添加胆固醇的天然成分饮食是用来诱导高胆固醇血症的。不同水平的胆固醇，脂肪和/或胆汁酸盐可以添加到众多的标准啮齿动物饮食之一，由EnvigoTeclad。在许多应用中，建议将这些成分添加到Envigo的最小到中等植物雌激素的全球啮齿动物饮食中。我们最小的植物雌激素全球啮齿动物饮食是不含豆粕的，限制了植物雌激素对你的研究结果的影响。豆粕是一种常见的植物雌激素来源，它可以减少主动脉脂肪条纹的发育，改善血浆胆固醇，从而降低动脉粥样硬化的风险。限制饮食豆粕可能会减少饮食诱导动脉粥样硬化模型中的混杂变量。联系营养学家讨论其他饮食选择。
添加胆固醇的最小和中度植物雌激素啮齿动物饮食的例子：

  • TD.1200971%胆固醇饮食(2020年-最小植物雌激素)
  • TD.078412%胆固醇饮食(2016年-最小植物雌激素)
  • TD.013832%胆固醇(2018年-中度植物雌激素)

研究用途：
在转基因和野生型模型中诱导高胆固醇血症而不促进肥胖。
主要饮食特征：

  • 标准的、以谷物为基础的啮齿动物饮食
  • 最小/中度植物雌激素饮食建议
  • 胆固醇(1-4%)

参考资料：

  1. 贝尔奇，J，等，对小鼠体内微血管内皮功能的纵向评估。Microvasc RES，2013年。85：P.86-92
  2. 哈特维森，K，等，饮食诱导高胆固醇血症小鼠模型研究动脉粥样硬化无肥胖和代谢综合征。Arteroscler Thromb VASc Biol，2007年。27(4)：P。878-85
兔子、仓鼠和猪是动脉粥样硬化的常见模型。请与营养师联系，了解有关信息和公式示例。看见兔子、猪和其他物种有关信息和公式示例。

Atherogenic

Diet can be a useful tool to induce or accelerate atherosclerosis in laboratory animal models.Key dietary features used to induce atherosclerosis in rodents vary depending on the research model, desired endpoint, and length of feeding.While formulations of atherogenic diets continue to evolve, the options that are well-described in the literature are summarized below.For more information on each diet option and literature references see the expandable tabs following the diet table.

Research use Key dietary features Examples
“Western” purified atherogenic diet
Accelerated hypercholesterolemia and plaque formation in genetically modified models such as Apoe and Ldlr deficient mice.
Used for diet induced obesity in a variety of rodent models.
  • High fat diet (20 – 23% by weight; 40 – 45% kcal from fat)
  • Saturated fatty acids (SFA >60% of total fatty acids)
  • Milkfat/butterfat
  • Sucrose (34% by weight)
  • Cholesterol (0.2% total)
 TD.88137
TD.10885
“Western” purified atherogenic diet with added cholesterol and cholate source*
Induce hypercholesterolemia and mild atherosclerosis (foam cells, fatty streaks) in primarily wild type mice and rats.
Will not promote obesity.
  • High fat diet (15 – 20% by weight; 34 – 45% kcal from fat)
  • Saturated fatty acids (SFA >55% of total fatty acids)
  • Milkfat/butterfat, cocoa butter
  • Sucrose (30-50% by weight)
  • Cholesterol (1 – 1.25%)
  • Cholate Source (0.5%)*
 TD.02028
TD.09237
Hybrid high fat diets with added cholesterol and cholate source*
Induce hypercholesterolemia and mild atherosclerosis (foam cells, fatty streaks) in primarily wild type mice and rats.
Will not promote obesity.
Also used for lithogenic (gallstone) rodent studies.
  • 75% rodent breeder diet; 25% purified ingredients
  • High fat (~15% by weight; 37% kcal from fat)
  • Saturated fatty acids (SFA >45% of total fatty acids)
  • Cholesterol (1.25%)
  • Cholate source (0.5%)*
 TD.88051
TD.90221
Standard diets with added cholesterol
Induce hypercholesterolemia in genetically modified and wild type models without promoting obesity.
  • Standard, grain-based rodent diet
  • Minimal/moderate phytoestrogen diets recommended
  • Cholesterol (1 – 4%)
 TD.120097
TD.07841
TD.01383

*Sodium cholate or cholic acid aid cholesterol and fat absorption and reduce cholesterol disposal via bile acid synthesis. However, if including a cholate source is not desired for your research, diets without cholate are available.

COLLAPSE ALL TABS

“Western” style diets are fed to genetically-modified cardiovascular models, such as Apoe and Ldlr deficient mice, to accelerate and enhance hypercholesterolemia and plaque formation and to elicit phenotypes commonly associated with metabolic syndrome. Within the atherogenic literature, a “Western” diet typically is described as a purified rodent diet with 20-23% milkfat/butterfat, 0.2% total cholesterol, and 34% sucrose by weight. TD.88137 is an example of a “Western” style diet that was originally designed to characterize and enhance atherosclerosis development in a newly generated Apoe-deficient mouse model. Contact us for more information about “Western” style diets, modifications, or possible control diets.
Examples:

  • TD.88137    Adjusted calories diet (42% from fat, 0.2% total cholesterol)
  • TD.10885    45% fat Kcal diet (0.2% total cholesterol)

Research use:
Accelerated hypercholesterolemia and plaque formation in genetically-modified models, such as Apoe and Ldlr deficient mice.
Used for diet-induced obesity in a variety of rodent models.
Key dietary features:

  • High Fat Diet (20-23% by weight; 40 – 45% kcal from fat)
  • Saturated fatty acids (SFA >60% of total fatty acids)
  • Milkfat/butterfat
  • Sucrose (34% by weight)
  • Cholesterol (0.2% total)

References:

  1. Febbraio, M., et al., Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice. J Clin Invest, 2000. 105(8): p. 1049-56.
  2. Huszar, D., et al., Increased LDL cholesterol and atherosclerosis in LDL receptor-deficient mice with attenuated expression of scavenger receptor B1. Arterioscler Thromb Vasc Biol, 2000. 20(4): p. 1068-73.
  3. Nakashima, Y., et al., ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree. Arterioscler Thromb, 1994. 14(1): p. 133-40.
  4. Nakashima, Y., et al., Upregulation of VCAM-1 and ICAM-1 at atherosclerosis-prone sites on the endothelium in the ApoE-deficient mouse. Arterioscler Thromb Vasc Biol, 1998. 18(5): p. 842-51.
  5. Plump, A.S., et al., Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells. Cell, 1992. 71(2): p. 343-53.
  6. Towler, D.A., et al., Diet-induced diabetes activates an osteogenic gene regulatory program in the aortas of low density lipoprotein receptor-deficient mice. J Biol Chem, 1998. 273(46): p. 30427-34.
  7. Tsuchiya, K., et al., FoxOs integrate pleiotropic actions of insulin in vascular endothelium to protect mice from atherosclerosis. Cell Metab, 2012. 15(3): p. 372-81.
Wild type mice and rats generally are resistant to atherosclerosis, requiring more extreme dietary manipulation to modify lipoprotein profiles and develop mild atherosclerosis (foam cells, fatty streaks). Modern formulations are made completely of purified ingredients because this more refined approach has been reported to decrease the incidence of gallstones and liver damage associated with less refined and more traditional dietary approaches. To induce mild atherosclerosis in wild type animals, the “Western” purified diet can be modified to increase cholesterol (1-1.25%) and add a bile salt such as sodium cholate or cholic acid. Contact us for more information, modifications, or possible control diets.
Examples of purified high fat diets with added cholesterol and cholate source*:

  • TD.02028    21% milkfat (1.25% cholesterol, 0.5% cholic acid)
  • TD.09237    15% milkfat diet (1% cholesterol, 0.5% sodium cholate)

Examples of purified high fat diets with added cholesterol (without cholate source):

  • TD.96121    21% milkfat (1.25% cholesterol)

Research Use:
Induce hypercholesterolemia and mild atherosclerosis (foam cells, fatty streaks) primarily in wild type mice and rats.
Will not promote obesity.
Key dietary features:

  • High fat diet (15-20% by weight; 34 – 45% kcal from fat)
  • Saturated fatty acids (SFA >55% of total fatty acids)
  • Milkfat/butterfat, cocoa butter
  • Sucrose (30-50% by weight)
  • Cholesterol (1 – 1.25%)
  • Cholate source (0.5%)*

References:

  1. Bernal, C., et al., Lipid biomarkers and metabolic effects of lycopene from tomato juice on liver of rats with induced hepatic steatosis. J Nutr Biochem, 2013. 24(11): p. 1870-81.
  2. Gao, Q., et al., Atherogenic diets exacerbate colitis in mice deficient in glutathione peroxidase. Inflamm Bowel Dis, 2010. 16(12): p. 2043-54.
  3. Lichtman, A.H., et al., Hyperlipidemia and atherosclerotic lesion development in LDL receptor-deficient mice fed defined semipurified diets with and without cholate. Arterioscler Thromb Vasc Biol, 1999. 19(8): p. 1938-44.
  4. Marcondes, M.C., et al., Effects of chronic mental stress and atherogenic diet on the immune inflammatory environment in mouse aorta. Brain Behav Immun, 2011. 25(8): p. 1649-57.
  5. Nishina, P.M., et al., Effects of dietary fats from animal and plant sources on diet-induced fatty streak lesions in C57BL/6J mice. J Lipid Res, 1993. 34(8): p. 1413-22.
  6. Nishina, P.M., et al., Atherosclerosis and plasma and liver lipids in nine inbred strains of mice. Lipids, 1993. 28(7): p. 599-605.
  7. Yue, P., et al., Enhanced hepatic apoA-I secretion and peripheral efflux of cholesterol and phospholipid in CD36 null mice. PLoS One, 2010. 5(3): p. e9906.
  8. Nishina, P.M., J. Verstuyft, and B. Paigen, Synthetic low and high fat diets for the study of atherosclerosis in the mouse. J Lipid Res, 1990. 31(5): p. 859-69.

*Sodium cholate or cholic acid aid cholesterol and fat absorption and reduce cholesterol disposal via bile acid synthesis. However, if including a cholate source is not desired for your research, diets without cholate are available. See TD.96121for a purified diet and TD.94059 for a hybrid diet. Contact us for additional options.

Beverly Paigen and colleagues first characterized atherosclerosis development in C57BL/6 mice by feeding a hybrid atherogenic diet. The hybrid diet was created by mixing a natural ingredient mouse diet in a 3:1 ratio with a concentrated purified diet (containing 5% cholesterol and 2% sodium cholate; referred to as Thomas-Hartroft diet). The resulting mixture recreated in TD.88051/TD.90221 (same formula) contains ~15.8% fat, 1.25% cholesterol, and 0.5% sodium cholate. This group later compared the hybrid atherogenic diet approach to the more modern “western” purified atherogenic diet with added cholesterol and cholate and found that the hybrid atherogenic diet induced more gallstones and liver damage. Hybrid diets contain a variety of unrefined ingredients that may modify lipid metabolism and atherogenesis and do not allow for precise control of ingredients and nutrients for the study of chronic diseases. Although more refined diets have been developed, hybrid atherogenic diets are still popular for inducing mild atherosclerosis and gallstones in wild type mice and rats. Contact us for more information, modifications, or possible control diets.
Examples of hybrid high-fat diets with added cholesterol and cholate source*:

  • TD.88051 and TD.90221 (same formula) are Teklad product codes for hybrid atherogenic diets

Example of hybrid high-fat diet with added cholesterol (without cholate source):

  • TD.94059

Research Use:
Induce hypercholesterolemia and mild atherosclerosis (foam cells, fatty streaks) primarily in wild type mice and rats.
Will not promote obesity.
Also used for lithogenic (gallstone) rodent studies.
Key dietary features:

  • 75% rodent breeder diet; 25% purified ingredients
  • High fat (~15% by weight; 37% kcal from fat)
  • Saturated fatty acids (SFA >45% of total fatty acids)
  • Cholesterol (1.25%)
  • Cholate source (0.5%)*

References:

  1. Nishina, P.M., J. Verstuyft, and B. Paigen, Synthetic low and high fat diets for the study of atherosclerosis in the mouse. J Lipid Res, 1990. 31(5): p. 859-69.
  2. Clee, S.M., et al., Plasma and vessel wall lipoprotein lipase have different roles in atherosclerosis. J Lipid Res, 2000. 41(4): p. 521-31.
  3. George, J., et al., Enhanced fatty streak formation in C57BL/6J mice by immunization with heat shock protein-65. Arterioscler Thromb Vasc Biol, 1999. 19(3): p. 505-10.
  4. Miyake, J.H., et al., Transgenic expression of cholesterol-7-alpha-hydroxylase prevents atherosclerosis in C57BL/6J mice. Arterioscler Thromb Vasc Biol, 2002. 22(1): p. 121-6.
  5. Paigen, B., et al., Quantitative assessment of atherosclerotic lesions in mice. Atherosclerosis, 1987. 68(3): p. 231-40.
  6. Schreyer, S.A., D.L. Wilson, and R.C. LeBoeuf, C57BL/6 mice fed high fat diets as models for diabetes-accelerated atherosclerosis. Atherosclerosis, 1998. 136(1): p. 17-24.
  7. Vergnes, L., et al., Cholesterol and cholate components of an atherogenic diet induce distinct stages of hepatic inflammatory gene expression. J Biol Chem, 2003. 278(44): p. 42774-84.

*Sodium cholate or cholic acid aid cholesterol and fat absorption and reduce cholesterol disposal via bile acid synthesis. However, if including a cholate source is not desired for your research, diets without cholate are available. See TD.96121for a purified diet and TD.94059 for a hybrid diet. Contact us for additional options.

Standard, natural ingredient diets with cholesterol added are fed to induce hypercholesterolemia. Various levels of cholesterol, fat, and/or bile salts can be added to one of the numerous standard rodent diets stocked by Envigo Teklad. For many applications, adding these components to Envigo’s minimal-to-moderate phytoestrogen global rodent diets is recommended. Our minimal phytoestrogen global rodent diets are soybean meal free, limiting the effect of phytoestrogens on your research outcomes. Soybean meal, a common dietary source of phytoestrogens, has been shown to decrease aortic fatty streak development and modify plasma cholesterol, which may reduce the risk of developing atherosclerosis. Limiting dietary soybean meal may reduce confounding variables within your dietary-induced atherosclerosis model. Contact a nutritionist to discuss additional diet options.
Examples of minimal and moderate phytoestrogen rodent diets with added cholesterol:

  • TD.120097  1% cholesterol diet (2020 – minimal phytoestrogens)
  • TD.07841    2% cholesterol diet (2016 – minimal phytoestrogens)
  • TD.01383    2% cholesterol (2018 – Moderate phytoestrogens)

Research use:
Induce hypercholesterolemia in genetically-modified and wild type models without promoting obesity.
Key dietary features:

  • Standard, grain-based rodent diet
  • Minimal/moderate phytoestrogen diets recommended
  • Cholesterol (1 – 4%)

References:

  1. Belch, J.J., et al., Longitudinal assessment of endothelial function in the microvasculature of mice in-vivo. Microvasc Res, 2013. 85: p. 86-92.
  2. Hartvigsen, K., et al., A diet-induced hypercholesterolemic murine model to study atherogenesis without obesity and metabolic syndrome. Arterioscler Thromb Vasc Biol, 2007. 27(4): p. 878-85.
Rabbits, hamsters, and swine are common models of atherosclerosis. Contact a nutritionist for information and formula examples. See rabbit, swine and other species for information and formula examples.