harlan teklad官網(wǎng)代理商 動物飼料 動脈粥樣硬化 膽固醇和膽酸 TD.88051

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harlan teklad官網(wǎng)代理商 動物飼料 動脈粥樣硬化 膽固醇和膽酸 TD.88051

harlan teklad官網(wǎng)代理商 動物飼料

動脈粥樣硬化

在實(shí)驗(yàn)動物模型中，飲食是誘導(dǎo)或加速動脈粥樣硬化的有用工具。用于誘發(fā)嚙齒類動物動脈粥樣硬化的主要飲食特征因研究模型、所需終點(diǎn)和喂養(yǎng)時(shí)間的不同而不同。盡管動脈粥樣硬化飲食的配方在不斷發(fā)展，但文獻(xiàn)中詳細(xì)描述的備選方案概述如下。有關(guān)每個(gè)飲食選項(xiàng)和文獻(xiàn)參考的更多信息，請參見節(jié)目表后面的可擴(kuò)展選項(xiàng)卡。

研究用途 主要飲食特征 實(shí)例
“西方”純正致動脈粥樣硬化飲食
加速高膽固醇血癥和斑塊形成的轉(zhuǎn)基因模型，如APOE和Ldlr缺乏的小鼠。用于飲食誘導(dǎo)肥胖的各種嚙齒動物模型。
  • 高脂飲食(按體重計(jì)算占20-23%；脂肪占40-45%)
  • 飽和脂肪酸(SFA>總脂肪酸的60%)
  • 乳脂/乳脂
  • 蔗糖(按重量計(jì)占34%)
  • 膽固醇(總數(shù)0.2%)
 TD.88137
TD.10885
添加膽固醇和膽酸來源的“西方”純動脈粥樣硬化飲食*
在野生型小鼠和大鼠中誘導(dǎo)高膽固醇血癥和輕度動脈粥樣硬化(泡沫細(xì)胞、脂肪條紋)。不會助長肥胖。
  • 高脂飲食(體重15-20%；脂肪34-45千卡)
  • 飽和脂肪酸(SFA>總脂肪酸的55%)
  • 乳脂/黃油、可可脂
  • 蔗糖(重量占30%-50%)
  • 膽固醇(1-1.25%)
  • 巧克力來源(0.5%)*
 TD.02028
TD.09237
添加膽固醇和膽酸鹽的混合高脂飲食*
在野生型小鼠和大鼠中誘導(dǎo)高膽固醇血癥和輕度動脈粥樣硬化(泡沫細(xì)胞、脂肪條紋)。不會助長肥胖。

也用于造石(膽石)嚙齒動物的研究。
  • 75%的嚙齒動物飼養(yǎng)員；25%的純化成分
  • 高脂肪(體重約15%；脂肪37%千卡)
  • 飽和脂肪酸(SFA>總脂肪酸的45%)
  • 膽固醇(1.25%)
  • 巧克力源(0.5%)*
 TD.88051
TD.90221
添加膽固醇的標(biāo)準(zhǔn)飲食
在轉(zhuǎn)基因和野生型模型中誘導(dǎo)高膽固醇血癥而不促進(jìn)肥胖。
  • 標(biāo)準(zhǔn)的、以谷物為基礎(chǔ)的嚙齒動物飲食
  • 最小/中度植物雌激素飲食建議
  • 膽固醇(1-4%)
 TD.120097
TD.07841
TD.01383

*膽酸鈉或膽酸有助膽固醇和脂肪的吸收，并可透過膽汁酸合成減少膽固醇的排出。然而，如果你的研究不想包括膽酸鹽的來源，沒有膽酸鹽的飲食是可用的。

折疊所有標(biāo)簽

“西式”飲食被喂給基因修飾的心血管模型，如APOE和Ldlr缺乏的小鼠，以加速和促進(jìn)高膽固醇血癥和斑塊形成，并引出通常與代謝綜合征相關(guān)的表型。在動脈粥樣硬化的文獻(xiàn)中，“西方”飲食通常被描述為含有20-23%乳脂/蝴蝶脂肪、0.2%總膽固醇和34%蔗糖的純嚙齒動物飲食。TD.88137這是一種“西式”飲食的例子，最初的目的是在一種新生成的APOE缺陷小鼠模型中描述和促進(jìn)動脈粥樣硬化的發(fā)展。聯(lián)系我們，以獲得更多關(guān)于“西方”風(fēng)格的飲食，修改，或可能的控制飲食。

例子：

  • TD.88137調(diào)整卡路里飲食(42%來自脂肪，0.2%總膽固醇)
  • TD.1088545%脂肪KCAL飲食(總膽固醇0.2%)

研究用途：

加速高膽固醇血癥和斑塊形成的轉(zhuǎn)基因模型，如APOE和Ldlr缺乏的小鼠。

用于飲食誘導(dǎo)肥胖的各種嚙齒動物模型。

主要飲食特征：

  • 高脂肪飲食(按體重計(jì)算占20-23%；脂肪占40-45%)
  • 飽和脂肪酸(SFA>總脂肪酸的60%)
  • 乳脂/乳脂
  • 蔗糖(按重量計(jì)占34%)
  • 膽固醇(總數(shù)0.2%)

參考資料：

  1. Febbraio，M，等人，B類清道夫受體CD 36的靶向性破壞對小鼠動脈粥樣硬化病變的發(fā)展有保護(hù)作用。j Clin Investment，2000年。105(8)：P。1049-56
  2. Huszar，D，等人，在低密度脂蛋白受體缺乏的小鼠體內(nèi)增加了低密度脂蛋白膽固醇和動脈粥樣硬化，減少了清道夫受體B1的表達(dá)。Arteroscler Thromb VASc Biol，2000年。20(4)：P。1068-73
  3. Nakashima，Y.，等人，ApoE缺乏的小鼠在整個(gè)動脈樹形成動脈粥樣硬化的各個(gè)階段的病變。Arteroscler Thromb，1994年。14(1)：P。133-40
  4. 中島，Y，等，VCAM-1和ICAM-1在ApoE缺乏的小鼠內(nèi)皮動脈粥樣硬化易發(fā)部位上調(diào)VCAM-1和ICAM-1的表達(dá)。Arteroscler Thromb VASc Biol，1998年。18(5)：P。842-51
  5. Plump，A.S.等人，ES細(xì)胞同源重組所致載脂蛋白E缺陷小鼠的嚴(yán)重高膽固醇血癥和動脈粥樣硬化。細(xì)胞，1992年。71(2)：P。343-53
  6. Towler，D.A.等，飲食誘導(dǎo)的糖尿病激活了低密度脂蛋白受體缺陷小鼠主動脈的成骨基因調(diào)控程序。j Biol Chem，1998年。273(46)：P。30427-34。
  7. Foxos整合胰島素在血管內(nèi)皮細(xì)胞中的多向性作用，以保護(hù)小鼠免受動脈粥樣硬化的影響。Metab細(xì)胞，2012年。15(3)：P。372-81。

野生型小鼠和大鼠一般對動脈粥樣硬化有抵抗力，需要更極端的飲食操作來改變脂蛋白譜，形成輕度動脈粥樣硬化(泡沫細(xì)胞、脂肪條紋)?，F(xiàn)代配方完全是由純化成分制成的，因?yàn)閾?jù)報(bào)道，這種更精細(xì)的方法可以減少較少精制和較傳統(tǒng)飲食方法引起的膽結(jié)石和肝臟損害的發(fā)生率。為了在野生型動物中誘導(dǎo)輕度動脈粥樣硬化，可對“西方”純化飼料進(jìn)行改良，以提高膽固醇(1-1.25%)，并添加膽酸鈉或膽酸等膽鹽。聯(lián)系我們獲得更多的信息，修改，或可能的控制飲食。

添加膽固醇和膽酸鹽來源的純化高脂飲食的例子*：

  • TD.0202821%乳脂(1.25%膽固醇，0.5%膽酸)
  • TD.0923715%乳脂飲食(1%膽固醇，0.5%膽酸鈉)

添加膽固醇的純化高脂飲食的例子(沒有膽酸來源)：

  • TD.9612121%乳脂(1.25%膽固醇)

研究用途：

主要在野生型小鼠和大鼠誘發(fā)高膽固醇血癥和輕度動脈粥樣硬化(泡沫細(xì)胞、脂肪條紋)。

不會助長肥胖。

主要飲食特征：

  • 高脂飲食(體重15-20%；脂肪34-45千卡)
  • 飽和脂肪酸(SFA>總脂肪酸的55%)
  • 乳脂/黃油、可可脂
  • 蔗糖(重量占30%-50%)
  • 膽固醇(1-1.25%)
  • 巧克力源(0.5%)*

參考資料：

  1. 番茄汁番茄紅素對大鼠肝臟脂肪變性的影響。j Nutr Biochem，2013年。24(11)：P。1870-81
  2. 高，Q，等，動脈粥樣硬化飲食加劇了小鼠缺乏谷胱甘肽過氧化物酶結(jié)腸炎。炎癥腸Dis，2010年。16(12)：P。2043-54
  3. Lichtman，A.H.，等，高脂血癥和動脈粥樣硬化病變的發(fā)展，低密度脂蛋白受體缺乏的小鼠，喂食定義半純化飲食與不含膽酸。Arteroscler Thromb VASc Biol，1999年。19(8)：P。1938-44年。
  4. 慢性精神應(yīng)激和致動脈粥樣硬化飲食對小鼠主動脈免疫炎癥環(huán)境的影響。BrainBehav Immun，2011年。25(8)：P。1649-57
  5. Nishina，P.m.，等，動物和植物來源的飲食脂肪對C57BL/6J小鼠因飲食引起的脂肪條紋損害的影響。j Lipid RES，1993年。34(8)：P。1413-22
  6. Nishina，P.m.，等，9種近交系小鼠動脈粥樣硬化及血漿和肝臟脂質(zhì)。脂質(zhì)，1993年。28(7)：P。599-605
  7. 月，P，等，增強(qiáng)CD 36空小鼠肝臟載脂蛋白A-I分泌及膽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，合成低脂和高脂肪飲食，用于研究小鼠動脈粥樣硬化。j Lipid RES，1990年。31(5)：P。859-69

*膽酸鈉或膽酸有助膽固醇和脂肪的吸收，并可透過膽汁酸合成減少膽固醇的排出。然而，如果你的研究不想包括膽酸鹽的來源，沒有膽酸鹽的飲食是可用的?？匆奣D.96121為了純正的飲食TD.94059混合飲食。請與我們聯(lián)系，了解其他選項(xiàng)。

貝弗利·派根和他的同事首先通過喂養(yǎng)一種混合性動脈粥樣硬化飲食來描述C57BL/6小鼠動脈粥樣硬化的發(fā)展。這種混合飼料是通過將一種天然成分的老鼠飼料按3：1的比例與濃縮的純化飼料(含5%膽固醇和2%膽酸鈉；稱為Thoms-Hartroft飲食)混合而成的。產(chǎn)生的混合物在TD.88051/TD.90221(同配方)含有~15.8%脂肪、1.25%膽固醇和0.5%膽酸鈉。這組人后來將混合動脈粥樣硬化飲食方法與更現(xiàn)代的“西方”純化動脈粥樣硬化飲食方法進(jìn)行了比較，并添加了膽固醇和膽酸鹽，發(fā)現(xiàn)混合動脈粥樣硬化飲食會導(dǎo)致更多的膽結(jié)石和肝臟損傷?；旌巷嬍澈卸喾N未精制的成分，這些成分可能會改變血脂代謝和動脈粥樣硬化的發(fā)生，并且不允許對成分和營養(yǎng)物進(jìn)行精確控制，以用于慢性病的研究。雖然已經(jīng)開發(fā)出了更精細(xì)的飲食，但混合動脈粥樣硬化飲食仍然是野生型小鼠和大鼠誘發(fā)輕度動脈粥樣硬化和膽結(jié)石的流行食品。聯(lián)系我們獲得更多的信息，修改，或可能的控制飲食。

添加膽固醇和膽酸鹽的混合高脂飲食實(shí)例*：

  • TD.88051和TD.90221(相同的配方)是特克拉德混合動脈粥樣硬化飲食的產(chǎn)品代碼。

添加膽固醇的混合高脂飲食的例子(沒有膽酸來源)：

  • TD.94059

研究用途：

主要在野生型小鼠和大鼠誘發(fā)高膽固醇血癥和輕度動脈粥樣硬化(泡沫細(xì)胞、脂肪條紋)。

不會助長肥胖。

也用于造石(膽石)嚙齒動物的研究。

主要飲食特征：

  • 75%的嚙齒動物飼養(yǎng)員；25%的純化成分
  • 高脂肪(體重約15%；脂肪37%千卡)
  • 飽和脂肪酸(SFA>總脂肪酸的45%)
  • 膽固醇(1.25%)
  • 巧克力源(0.5%)*

參考資料：

  1. Nishina，下午，J.Verstuyft，B.Paigen，合成低脂和高脂肪飲食，用于研究小鼠動脈粥樣硬化。j Lipid RES，1990年。31(5)：P。859-69
  2. Clee，S.M.，等，血漿和血管壁脂蛋白脂肪酶在動脈粥樣硬化中有不同的作用。j Lipid RES，2000年。41(4)：P。521-31
  3. George，J.等人，用熱休克蛋白-65免疫C57BL/6J小鼠，促進(jìn)了脂肪條紋的形成。Arteroscler Thromb VASc Biol，1999年。19(3)：P。505-10
  4. Miyake，J.H.，等，膽固醇-7-α-羥化酶基因表達(dá)對C57BL/6J小鼠動脈粥樣硬化的預(yù)防作用。Arteroscler Thromb VASc Biol，2002年。22(1)：P。121-6
  5. Paigen，B，等，小鼠動脈粥樣硬化病變的定量評估。動脈粥樣硬化，1987年。68(3)：P。231-40。
  6. Schreyer，S.A.，D.L.Wilson和R.C.LeBoeuf，C57BL/6小鼠以高脂飲食作為糖尿病加速動脈粥樣硬化的模型。動脈粥樣硬化，1998年。136(1)：P。17-24。
  7. Vergnes，L，等，膽固醇和膽酸組成的動脈粥樣硬化飲食誘導(dǎo)不同階段的肝臟炎癥基因的表達(dá)。j Biol Chem，2003年。278(44)：P。42774-84。

*膽酸鈉或膽酸有助膽固醇和脂肪的吸收，并可透過膽汁酸合成減少膽固醇的排出。然而，如果你的研究不想包括膽酸鹽的來源，沒有膽酸鹽的飲食是可用的?？匆奣D.96121為了純正的飲食TD.94059混合飲食。請與我們聯(lián)系，了解其他選項(xiàng)。

標(biāo)準(zhǔn)的，添加膽固醇的天然成分飲食是用來誘導(dǎo)高膽固醇血癥的。不同水平的膽固醇，脂肪和/或膽汁酸鹽可以添加到眾多的標(biāo)準(zhǔn)嚙齒動物飲食之一，由EnvigoTeclad。在許多應(yīng)用中，建議將這些成分添加到Envigo的最小到中等植物雌激素的全球嚙齒動物飲食中。我們最小的植物雌激素全球嚙齒動物飲食是不含豆粕的，限制了植物雌激素對你的研究結(jié)果的影響。豆粕是一種常見的植物雌激素來源，它可以減少主動脈脂肪條紋的發(fā)育，改善血漿膽固醇，從而降低動脈粥樣硬化的風(fēng)險(xiǎn)。限制飲食豆粕可能會減少飲食誘導(dǎo)動脈粥樣硬化模型中的混雜變量。聯(lián)系營養(yǎng)學(xué)家討論其他飲食選擇。

添加膽固醇的最小和中度植物雌激素嚙齒動物飲食的例子：

  • TD.1200971%膽固醇飲食(2020年-最小植物雌激素)
  • TD.078412%膽固醇飲食(2016年-最小植物雌激素)
  • TD.013832%膽固醇(2018年-中度植物雌激素)

研究用途：

在轉(zhuǎn)基因和野生型模型中誘導(dǎo)高膽固醇血癥而不促進(jìn)肥胖。

主要飲食特征：

  • 標(biāo)準(zhǔn)的、以谷物為基礎(chǔ)的嚙齒動物飲食
  • 最小/中度植物雌激素飲食建議
  • 膽固醇(1-4%)

參考資料：

  1. 貝爾奇，J，等，對小鼠體內(nèi)微血管內(nèi)皮功能的縱向評估。Microvasc RES，2013年。85：P.86-92
  2. 哈特維森，K，等，飲食誘導(dǎo)高膽固醇血癥小鼠模型研究動脈粥樣硬化無肥胖和代謝綜合征。Arteroscler Thromb VASc Biol，2007年。27(4)：P。878-85

兔子、倉鼠和豬是動脈粥樣硬化的常見模型。請與營養(yǎng)師聯(lián)系，了解有關(guān)信息和公式示例?？匆娡米印⒇i和其他物種有關(guān)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.