harlan teklad官網(wǎng) 動(dòng)物飼料 TD.88137調(diào)整卡路里飲食 TD.1088545%脂肪KCAL飲食
“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(dòng)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(dòng)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(dòng)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：
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(dòng)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：
- Febbraio，M，等人，B類清道夫受體CD 36的靶向性破壞對(duì)小鼠動(dòng)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
- 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(dòng)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
- Nakashima，Y.，等人，ApoE缺乏的小鼠在整個(gè)動(dòng)脈樹形成動(dòng)脈粥樣硬化的各個(gè)階段的病變。Arteroscler Thromb，1994年。14(1)：P。133-40
- 中島，Y，等，VCAM-1和ICAM-1在ApoE缺乏的小鼠內(nèi)皮動(dòng)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
- 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(dòng)脈粥樣硬化。細(xì)胞，1992年。71(2)：P。343-53
- 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乏小鼠主動(dòng)脈的成骨基因調(diào)控程序。j Biol Chem，1998年。273(46)：P。30427-34。
- 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(dòng)脈粥樣硬化的影響。Metab細(xì)胞，2012年。15(3)：P。372-81。
“Western” purified atherogenic diet
“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:
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.