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Hayek(TD88137)西方饮食模型饲料介绍
Hayek Diet(TD88137)for Western Diet Model

一、Hayek模型饲料


请注意
西方饮食模型饲料是一个大的概念,只要是高脂、高糖、高胆固醇等其中某2项或三项都称为西方饮食模型饲料。本页介绍的TD88137虽然被命名为西方饮食模型饲料,但只是西方饮食模型饲料中的一种。

Hayek等早在90年代早期研究时进行人类脂蛋白转基因鼠的研究,所设计的西方饮食模型饲料主要是脂肪21.2%,碳水化合物49.1%,蛋白质19.8%,胆固醇0.2%。这个模型饲料的特点是脂肪全部是奶油,虽然也是高胆固醇,但是胆固醇含量只有0.2%,不像Paigen饲料中用到1.25%,而且其中不添加胆盐。所采用的这个模型饲料在Harlan(Teklad)公司生产,编号为TD88137。

很显然,基于对这个模型饲料的最大贡献,应该叫做Hayek模型饲料,但是,文献中都叫做TD88137。

与ResearchDiets公司相比,Harlan公司的做法有些欠妥。ResearchDiet公司在与van Heek等研究者合作时诞生的45%高脂肥胖饲料(D12451),后来又在此基础上制作的60%高脂肥胖饲料(D12492)都是以van Heek来称呼的,叫做van Heek系列模型饲料,这显然是肯定了van Heek的贡献。然而,Harlan公司与Hayek等研究者合作的西方饮食模型饲料(TD88137),在介绍TD88137时只是说他们公司与某某某大学的研究者们合作,没有具体说明哪些研究者。这也许是至今很少有论文中提及Haylek(甚至很多研究中没有引用Haylek等的研究论文)的原因。

Hayek西方饮食模型饲料的用途、缺点
Hayek西方饮食模型饲料的用途:

广泛应用于大小鼠肥胖模型高血脂模型高胆固醇血症模型胰岛素抵抗模型II型糖尿病模型代谢综合症模型非酒精性脂肪肝模型动脉粥样硬化模型高同型半胱氨酸血症模型,等等。请注意不同种系和品系的差异。

Hayek西方饮食模型饲料的缺点:

(1)营养素不合理,需要优化;

二、Hayek模型饲料的用途和缺点


Hayek模型饲料已经在大鼠和小鼠等不同动物中使用,广泛应用于多种西方饮食疾病的研究,见右图。

当今很多著名实验动物饲料企业都生产Hayek模型饲料。除了Harlan(Teklad)公司生产的TD88137,其他公司的情况是:ResearchDiets是D12079B。

在国内,特洛菲饲料科技有限公司采取了优化(TP26301, TP26302)、不优化(TP26300)和重新设计(TP26302和TP26304)三种策略提供不同的高脂肥胖模型饲料供研究者选用,并且提供了各种匹配的对照饲料供研究者根据研究的具体情况选择。

如果读者准备使用Hayek饲料开展研究,请阅读“Hayek(TD88137)西方饮食模型饲料存在的问题和纠正”。

 

References:

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[11] Cash JG, Kuhel DG, Basford JE, Jaeschke A, Chatterjee TK, Weintraub NL, Hui DY. Apolipoprotein E4 Impairs Macrophage Efferocytosis and Potentiates Apoptosis by Accelerating Endoplasmic Reticulum Stress. J Biol Chem. 2012 August 10; 287(33): 27876–27884.

[12] Szeto FL, Reardon CA, Yoon D, Wang Y, Wong KE, Chen Y, Kong J, Liu SQ, Thadhani R, Getz GS, Li YC. Vitamin D Receptor Signaling Inhibits Atherosclerosis in Mice. Mol Endocrinol. 2012 July; 26(7): 1091–1101.

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[14] Kraja AT, Lawson HA, Arnett DK, Borecki IB, Broeckel U, de las Fuentes L, Hunt SC, Province MA, Cheverud J, Rao DC. Obesity–insulin targeted genes in the 3p26-25 region in human studies and LG/J and SM/J mice. Metabolism. Metabolism. 2012 August; 61(8): 1129–1141.

[15] Rohwedder I, Montanez E, Beckmann K, Bengtsson E, Dunér P, Nilsson J, Soehnlein O, Fässler R. Plasma fibronectin deficiency impedes atherosclerosis progression and fibrous cap formation. EMBO Mol Med. 2012 July; 4(7): 564–576.

[16] Lee J, Seok S, Yu P, Kim K, Smith Z, Rivas-Astroza M, Zhong S, Kemper JK. Genomic analysis of hepatic Farnesoid X Receptor (FXR) binding sites reveals altered binding in obesity and direct gene repression by FXR Hepatology. Hepatology. 2012 July; 56(1): 108–117.

[17] Ding L, Biswas S, Morton RE, Smith JD, Hay N, Byzova TV, Febbraio M, Podrez EA. Akt3 Deficiency in Macrophages Promotes Foam Cell Formation and Atherosclerosis in Mice.Cell Metab. 2012 June 6; 15(6): 861–872

[18] Navab M, Reddy ST, Anantharamaiah GM, Hough G, Buga GM, Danciger J, Fogelman AM. D-4F-mediated reduction in metabolites of arachidonic and linoleic acids in the small intestine is associated with decreased inflammation in low-density lipoprotein receptor-null mice. J Lipid Res. 2012 March; 53(3): 437–445.

[19] Zhang X, Thatcher SE, Rateri DL, Bruemmer D, Charnigo R, Daugherty A, Cassis LA. Transient Exposure of Neonatal Female Mice to Testosterone Abrogates the Sexual Dimorphism of Abdominal Aortic Aneurysms. Circ Res. 2012 May 25; 110(11): e73–e85

[20] Fox RG, Magness S, Kujoth GC, Prolla TA, Maeda N. Mitochondrial DNA polymerase editing mutation, PolgD257A, disturbs stem-progenitor cell cycling in the small intestine and restricts excess fat absorption. Am J Physiol Gastrointest Liver Physiol. 2012 May 1; 302(9): G914–G924

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[25] Yoshino J, Mills KF, Yoon MJ, Imai S. Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011 October 5; 14(4): 528–536.

[26] Rahaman SO, Swat W, Febbraio M, Silverstein RL. Vav Family Rho Guanine Nucleotide Exchange Factors Regulate CD36-mediated Macrophage Foam Cell Formation. J Biol Chem. 2011 March 4; 286(9): 7010–7017.

[27] Maher JJ. New Insights from Rodent Models of Fatty Liver Disease. Antioxid Redox Signal. 2011 July 15; 15(2): 535–550.

[28] Wan W, Lim JK, Lionakis MS, Rivollier A, McDermott DH, Kelsall BL, Farber JM, Murphy PM. Genetic Deletion of Chemokine Receptor Ccr6 Decreases Atherogenesis in ApoE-deficient Mice. Circ Res. 2011 August 5; 109(4): 374–381.

[29] Li J, Wang Q, Chai W, Chen MH, Liu Z, Shi W. Hyperglycemia in apolipoprotein E-deficient mouse strains with different atherosclerosis susceptibility. Cardiovasc Diabetol. 2011; 10: 117.

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有困惑?那就商量呗!

高脂肥胖、代谢综合症、胰岛素抵抗、高血脂(高甘油三酯血症、高胆固醇血症)、糖尿病、动脉粥样硬化、非酒精性脂肪肝,等模型饲料

南通特洛菲饲料科技有限公司提供各种动物、各种类型的肥胖及其并发症的模型饲料。以下介绍与TD88137相当或者优化、重新设计的西方饮食模型饲料。

---------《》-------

大鼠小鼠西方饮食模型饲料:

markerTP26300

与Harlan公司TD88137相当。为追求与原作者使用的TD88137的研究者设计。用于未成年。

markerTP26301

由于TD88137的必需脂肪酸过少, TP26301进行了优化,与ResearchDiets公司D12079B相当。用于未成年。

markerTP26302

TD88137的营养素不科学、不合理, TP26302进行了优化。用于未成年期。

markerTP26303

TP26303针对TD88137进行了全面优化,用于未成年期。

markerTP26304

由于TD88137不适合成年期喂养, TP26304在TD88137基础上专为成年期设计。营养素符合成年期要求。

markerTP26305

TP26305专为成年期设计,避免必需脂肪酸过低,又营养素合理。

 详细情况,请浏览Hayek西方饮食模型饲料(Hayek Western-type Diet)选择指南




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